Immunobiology: the immune system in health and disease
Gespeichert in:
| Format: | Buch |
|---|---|
| Sprache: | English |
| Veröffentlicht: |
New York, NY [u.a.]
Garland Science
2005
|
| Ausgabe: | 6. ed. |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | CD-ROM u.d.T.: Immunobiology interactive. - 7. Aufl. u.d.T.: Murphy, Kenneth: Janeway's immunobiology |
| Beschreibung: | XXIII, 823 S. zahlr. Ill., graph. Darst. 1 CD-ROM (12 cm) |
| ISBN: | 0443073090 0815341016 0443073104 |
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| 245 | 1 | 0 | |a Immunobiology |b the immune system in health and disease |c Charles A. Janeway ... |
| 246 | 1 | 3 | |a Immunobiology interactive |
| 250 | |a 6. ed. | ||
| 264 | 1 | |a New York, NY [u.a.] |b Garland Science |c 2005 | |
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Datensatz im Suchindex
| _version_ | 1804130560987103232 |
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| adam_text | PART I 1 AN INTRODUCTION TO IMMUNOBIOLOGY AND INNATE IMMUNITY
Chapter 1 Basic Concepts in Immunology 1
Chapter 2 Innate Immunity 37
PART II I THE RECOGNITION OF ANTIGEN
Chapter 3 Antigen Recognition by B cell and T cell Receptors 103
Chapter 4 The Generation of Lymphocyte Antigen Receptors 135
Chapter 5 Antigen Presentation to T Lymphocytes 169
PART III | THE DEVELOPMENT OF MATURE LYMPHOCYTE RECEPTOR
REPERTOIRES
Chapter 6 Signaling Through Immune System Receptors 203
Chapter 7 The Development and Survival of Lymphocytes 241
?iNWT^ THE ADAPTIVE IMMUNE RESPONSE
Chapter 8 T Cell Mediated Immunity 319
Chapter 9 The Humoral Immune Response 367
Chapter 10 Adaptive Immunity to Infection 409
PARTV | THE IMMUNE SYSTEM IN HEALTH AND DISEASE
Chapter 11 Failures of Host Defense Mechanisms 461
Chapter 12 Allergy and Hypersensitivity 517
Chapter 13 Autoimmunity and Transplantation 557
Chapter 14 Manipulation of the Immune Response 613
PART VI I THE ORIGINS OF IMMUNE RESPONSES
Chapter 15 Evolution of the Innate Immune System 665
Appendix I Immunologists Toolbox 683
Appendix II CD Antigens 731
Appendix III Cytokines and their Receptors 747
Appendix IV Chemokines and their Receptors 750
Appendix V Immunological Constants 751
Biographies 752
Glossary 753
Index 778
Detailed Contents
Parti I AN INTRODUCTION TO IMMUNO
1 BIOLOGY AND INNATE IMMUNITY
Chapter 1 Basic Concepts in Immunology 1
The components of the immune system. 2
1 1 The white blood cells of the immune system derive from
precursors in the bone marrow. 3
1 2 Lymphocytes mature in the bone marrow or the thymus. 7
1 3 The peripheral lymphoid organs are specialized to trap
antigen bearing dendritic cells, to allow initiation of adaptive
immune responses, and to provide signals that sustain
recirculating lymphocytes. 8
1 4 Lymphocytes circulate between blood and lymph. 10
Summary. 11
Principles of innate and adaptive immunity. 12
1 5 Most infectious agents induce inflammatory responses by
activating innate immunity. 12
1 6 Activation of specialized antigen presenting cells is a
necessary first step for induction of adaptive immunity. 13
1 7 The innate immune system provides an initial discrimination
between self and nonself. 14
1 8 Lymphocytes activated by antigen give rise to clones of
antigen specific cells that mediate adaptive immunity. 15
1 9 Clonal selection of lymphocytes is the central principle of
adaptive immunity. 16
1 10 The structure of the antibody molecule illustrates the central
puzzle of adaptive immunity. 17
1 11 Each developing lymphocyte generates a unique antigen
receptor by rearranging its receptor gene segments. 17
1 12 Development and survival of lymphocytes are determined by
signals received through their antigen receptors. 18
1 13 Lymphocytes proliferate in response to antigen in peripheral
lymphoid organs, generating effector cells and immuno
logical memory. 19
1 14 Interaction with other cells as well as with antigen is nec¬
essary for lymphocyte activation. 21
Summary. 22
The recognition and effector mechanisms of adaptive
immunity. 24
1 15 Antibodies deal with extracellular forms of pathogens and
their toxic products. 25
1 16 T cells are needed to control intracellular pathogens and to
activate B cell responses to most antigens. 26
1 17 T cells are specialized to recognize foreign antigens as pep
tide fragments bound to proteins of the major histocomp
atibility complex. 28
1 18 Two major types of T cell recognize peptides bound to prot¬
eins of two different classes of MHC molecule. 29
1 19 Defects in the immune system result in increased suscept¬
ibility to infection. 31
1 20 Understanding adaptive immune responses is important for
the control of allergies, autoimmune disease, and organ graft
rejection. 32
1 21 Vaccination is the most effective means of controlling
infectious diseases. 33
Summary. 33
Summary to Chapter 1. 34
Chapter 2 Innate Immunity 37
The front line of host defense. 38
2 1 Infectious agents must overcome innate host defenses to
establish a focus of infection. 39
2 2 The epithelial surfaces of the body make up the first lines of
defense against infection. 40
2 3 After entering tissues, many pathogens are recognized,
ingested, and killed by phagocytes. 42
2 4 Pathogen recognition and tissue damage initiate an
inflammatory response. 45
Summary. 48
Pattern recognition in the innate immune system. 48
2 5 Receptors with specificity for pathogen molecules recognize
patterns of repeating structural motifs. 49
2 6 Receptors on phagocytes can signal the presence of
pathogens. 51
2 7 Each of the 10 Toll like receptors in humans recognizes
a particular molecular structure that is present in many
pathogens. 51
2 8 The effects of bacterial lipopolysaccharide on macrophages
are mediated by CD14 binding to TLR 4. 52
2 9 Activation of Toll like receptors triggers the production of pro
inflammatory cytokines and chemokines, and the expression
of co stimulatory molecules. 53
Summary. 54
The complement system and innate immunity. 55
2 10 Complement is a system of plasma proteins that interacts
with pathogens to mark them for destruction by phagocytes. 56
2 11 The classical pathway is initiated by activation of the C1
complex. 58
2 12 The mannose binding lectin pathway is homologous to the
classical pathway. 60
2 13 Complement activation is largely confined to the surface on
which it is initiated. 61
2 14 Hydrolysis of C3 causes initiation of the alternative pathway
of complement. 61
2 15 Surface bound C3 convertase deposits large numbers of
C3b fragments on pathogen surfaces and generates C5
convertase activity. 66
2 16 Ingeslion of complement tagged pathogens by phagocytes is
mediated by receptors for the bound complement proteins. 66
2 17 Small fragments of some complement proteins can initiate
a local inflammatory response. 68
2 18 The terminal complement proteins polymerize to form pores
in membranes that can kill certain pathogens. 69
2 19 Complement control proteins regulate all three pathways of
complement activation and protect the host from its
destructive effects. 70
Summary. 75
Induced innate responses to infection. 75
2 20 Activated macrophages secrete a range of cytokines that
have a variety of local and distant effects. 76
2 21 Chemokines released by phagocytes and dendritic cells
recruit cells to sites of infection. 77
2 22 Cell adhesion molecules control interactions between
leukocytes and endothelial cells during an inflammatory
response. 80
2 23 Neutrophils make up the first wave of cells that cross the
blood vessel wall to enter inflammatory sites. 82
2 24 Tumor necrosis factorAalpha is an important cytokine that
triggers local containment of infection but induces shock
when released systemically. 84
2 25 Cytokines released by phagocytes activate the acute phase
response. 85
2 26 Interferons induced by viral infection make several
contributions to host defense. 87
2 27 NK cells are activated by interferons and macrophage
derived cytokines to serve as an early defense against
certain intracellular infections. 89
2 28 NK cells possess receptors for self molecules that prevent
their activation by uninfected cells. 90
2 29 Several lymphocyte subpopulations behave as innate like
lymphocytes. 93
Summary. 95
Summary to Chapter 2. 95
Part II | THE RECOGNITION OF ANTIGEN
Chapter 3 Antigen Recognition by B cell and
T cell Receptors 103
The structure of a typical antibody molecule. 104
3 1 IgG antibodies consist of four polypeptide chains. 105
3 2 Immunoglobulin heavy and light chains are composed of
constant and variable regions. 106
3 3 The antibody molecule can readily be cleaved into funct¬
ionally distinct fragments. 106
3 4 The immunoglobulin molecule is flexible, especially at the
hinge region. 108
3 5 The domains of an immunoglobulin molecule have similar
structures. 109
Summary. 110
The interaction of the antibody molecule with specific
antigen. 110
3 6 Localized regions of hypervariable sequence form the
antigen binding site. 110
3 7 Antibodies bind antigens via contacts with amino acids in
CDRs, but the details of binding depend upon the size
and shape of the antigen. 112
3 8 Antibodies bind to conformational shapes on the surfaces
of antigens. 112
3 9 Antigen antibody interactions involve a variety of forces. 113
Summary. 115
Antigen recognition by T cells. 115
3 10 The antigen receptor on T cells is very similar to a Fab
fragment of immunoglobulin. 116
3 11 A T cell receptor recognizes antigen in the form of a
complex of a foreign peptide bound to an MHC molecule. 117
3 12 T cells with different functions are distinguished by CD4
and CD8 cell surface proteins and recognize peptides bound
to different classes of MHC molecule. 118
3 13 The two classes of MHC molecule are expressed differen¬
tially on cells. 120
3 14 The two classes of MHC molecule have distinct subunit
structures but similar three dimensional structures. 121
3 15 Peptides are stably bound to MHC molecules, and also
serve to stabilize the MHC molecule on the cell surface. 124
3 16 MHC class I molecules bind short peptides of 8 10 amino
acids by both ends. 125
3 17 The length of the peptides bound by MHC class II molecules
is not constrained. 126
3 18 The crystal structures of several MHC:peptide:T cell receptor
complexes all show the same T cell receptor orientation over
the MHC:peptide complex. 128
3 19 A distinct subset of T cells bears an alternative receptor
made up of y and 5 chains. 129
Summary. 130
Summary to Chapter 3. 130
Chapter 4 The Generation of Lymphocyte
Antigen Receptors 135
The generation of diversity in immunoglobulins. 136
4 1 Immunoglobulin genes are rearranged in antibody producing
cells. 136
4 2 Complete genes that encode a V region are generated by
the somatic recombination of separate gene segments. 137
4 3 For each immunoglobulin chain, multiple V region gene
segments are present on one contiguous stretch of
chromosome. 138
4 4 Rearrangement of V, D, and J gene segments is guided by
flanking ONA sequences. 140
4 5 The reaction that recombines V, D, and J gene segments
involves both lymphocyte specific and ubiquitous DNA
modifying enzymes. 142
4 6 The diversity of the immunoglobulin repertoire is generated
by four main processes. 144
4 7 The multiple inherited gene segments are used in different
combinations. 144
4 8 Variable addition and subtraction of nucleotides at the
junctions between gene segments contributes to the
diversity of the third hypervariable region. 145
4 9 Rearranged V genes are further diversified by somatic
hypermutation. 146
4 10 In some species, most immunoglobulin gene diversification
occurs after gene rearrangement. 148
Summary. 148
T cell receptor gene rearrangement. 149
4 11 The T cell receptor gene segments are arranged in a
similar pattern to immunoglobulin gene segments and are
rearranged by the same enzymes. 149
4 12 T cell receptors concentrate diversity in the third
hypervariable region. 151
4 13 j.§ T cell receptors are also generated by gene
rearrangement. 152
4 14 Somatic hypermutation does not generate diversity in T cell
receptors. 153
Summary. 153
Structural variation in immunoglobulin constant regions. 154
4 15 Transmembrane and secreted forms of immunoglobulin are
generated from alternative heavy chain transcripts. 154
4 16 The immunoglobulin heavy chain isotypes are distinguished
by the structure of their constant regions. 156
4 17 Mature naive B cells express both IgM and IgD at their
surface. 157
4 18 Isotype switching enables the same assembled Vh exon
to be associated with different Ch genes in the course of
an immune response. 158
4 19 Antibody C regions confer functional specialization. 160
4 20 IgM and IgA can form polymers. 162
4 21 Various differences between immunoglobulins can be
detected by antibodies. 163
Summary. 164
Summary to Chapter 4. 164
Chapter 5 Antigen Presentation to
T Lymphocytes 169
The generation of T cell receptor ligands. 170
5 1 The MHC class I and class II molecules deliver peptides
to the cell surface from two distinct intracellular
compartments. 170
5 2 Peptides that bind to MHC class I molecules are actively
transported from the cytosol to the endoplasmic reticulum. 171
5 3 Peptides for transport into the endoplasmic reticulum are
generated in the cytosol. 172
5 4 Newly synthesized MHC class I molecules are retained
in the endoplasmic reticulum until they bind peptide. 174
5 5 Peptides presented by MHC class II molecules are
generated in acidified endocytic vesicles. 176
5 6 The invariant chain directs newly synthesized MHC
class II molecules to acidified intracellular vesicles. 178
5 7 A specialized MHC class ll like molecule catalyzes
loading of MHC class II molecules with peptides. 179
5 8 Stable binding of peptides by MHC molecules provides
effective antigen presentation at the cell surface. 181
Summary. 182
The major histocompatibility complex and its functions. 183
5 9 Many proteins involved in antigen processing and
presentation are encoded by genes within the major
histocompatibility complex. 183
5 10 A variety of genes with specialized functions in immunity
are also encoded in the MHC. 185
5 11 Specialized MHC class I molecules act as ligands for the
activation and inhibition of NK cells. 187
5 12 The protein products of MHC class I and class II genes
are highly polymorphic. 187
5 13 MHC polymorphism affects antigen recognition by T cells
by influencing both peptide binding and the contacts
between T cell receptor and MHC molecule. 189
5 14 Nonself MHC molecules are recognized by 1 10%
of T cells. 192
5 15 Many T cells respond to superantigens. 193
5 16 MHC polymorphism extends the range of antigens to
which the immune system can respond. 194
5 17 MHC polymorphism is generated by several different
genetic processes. 195
5 18 Some peptides and lipids generated in the endocytic
pathway can be bound by MHC class Hike molecules
that are encoded outside the MHC. 196
Summary. 197
Summary to Chapter 5. 197
Part III I THE DEVELOPMENT OF MATURE
1 LYMPHOCYTE RECEPTOR
REPERTOIRES
Chapter 6 Signaling Through Immune System
Receptors 203
General principles of transmembrane signaling. 204
6 1 Binding of antigen leads to clustering of antigen receptors
on lymphocytes. 204
6 2 Clustering of antigen receptors leads to activation of
intracellular signal molecules. 206
6 3 Receptors and signaling molecules concentrate in
specialized regions of the cell membrane. 206
6 4 Phosphorylation of receptor cytoplasmic tails by tyrosine
kinases concentrates intracellular signaling molecules
around the receptors. 208
6 5 Intracellular signaling components recruited to activated
receptors transmit the signal onward from the membrane
and amplify it. 209
6 6 Small G proteins activate a protein kinase cascade that
transmits the signal to the nucleus. 211
Summary. 212
Antigen receptor structure and signaling pathways. 212
6 7 The variable chains of lymphocyte antigen receptors are
associated with invariant accessory chains that perform the
signaling function of the receptor. 213
6 8 The ITAMs associated with the B cell and T cell receptors
are phosphorylated by protein tyrosine kinases of the
Src family. 214
6 9 Antigen receptor signaling is enhanced by co receptors
that bind the same ligand. 216
6 10 Fully phosphorylated ITAMs bind the protein tyrosine
kinases Syk and ZAP 70 and enable them to be
activated. 218
6 11 Downstream events are mediated by proteins that
associate with the phosphorylated tyrosines, and bind
to and activate other proteins. 218
6 12 Antigen recognition leads ultimately to the induction of
new gene synthesis by activating transcription factors. 221
6 13 Signals from the antigen receptor alter the cytoskeleton
to produce changes in cell shape, motility, and secretion. 224
6 14 Not all ligands for the T cell receptor produce a similar
response. 224
6 15 Other receptors on leukocytes also use ITAMs to signal
activation. 226
6 16 Antigen receptor signaling can be inhibited by receptors
associated with ITIMs. 226
Summary. 227
Other signaling pathways that contribute to lymphocyte
behavior. 228
6 17 Microbes and their products release NFkB from its
site in the cytosol through an ancient pathway of host
defense against infection. 228
6 18 Bacterial peptides, mediators of inflammatory responses,
and chemokines signal through members of the G protein
coupled receptor family. 230
6 19 Cytokines signal lymphocytes by binding to cytokine
receptors and triggering Janus kinases to phosphorylate
and activate STAT proteins. 231
6 20 Programmed cell death of activated lymphocytes is
triggered mainly through the receptor Fas. 232
6 21 Lymphocyte survival is maintained by a balance between
death promoting and death inhibiting members of the Bcl 2
family of proteins. 233
6 22 Homeostasis of lymphocyte populations is maintained
by signals that lymphocytes are continually receiving
through their antigen receptors. 234
Summary. 236
Summary to Chapter 6. 236
Chapter 7 The Development and Survival of
Lymphocytes 241
Generation of lymphocytes in bone marrow and
thymus. 244
7 1 Lymphocyte development occurs in specialized
environments and is regulated by signals from the
environment along with the somatic rearrangement
of the antigen receptor genes. 245
7 2 B cells develop in the bone marrow with the help of
stromal cells and achieve maturity in peripheral lymphoid
organs. 247
7 3 Stages in B cell development are distinguished by the
expression of immunoglobulin chains and particular
cell surface proteins. 248
7 4 T cells also originate in the bone marrow, but all the
important events in their development occur in the thymus. 251
7 5 T cell precursors proliferate extensively in the thymus but
most die there. 253
7 6 Successive stages in the development of thymocytes
are marked by changes in cell surface molecules. 254
7 7 Thymocytes at different developmental stages are found
in distinct parts of the thymus. 256
Summary. 257
The rearrangement of antigen receptor gene segments
controls lymphocyte development. 258
7 8 B cells undergo a programmed series of gene
rearrangements in the bone marrow. 258
7 9 Successful rearrangement of heavy chain immunoglobulin
gene segments leads to the formation of a pre B cell
receptor that halts further VH to DJH rearrangement
and triggers the cell to divide. 260
7 10 Rearrangement at the immunoglobulin light chain locus
leads to cell surface expression of the B cell receptor. 262
7 11 The expression of proteins regulating immunoglobulin gene
rearrangement and function is developmentally programmed. 264
7 12 T cells in the thymus undergo a series of gene segment
rearrangements similar to those of B cells. 267
7 13 Successful rearrangement at the (3 chain locus and synth¬
esis of a p chain leads to the production of a pre T cell
receptor that triggers cell proliferation and cessation of
P chain gene rearrangement. 267
7 14 T cell a chain genes undergo successive rearrangements
until positive selection or cell death intervenes. 270
7 15 T cells with oc:p or y:5 receptors arise from a common
progenitor. 272
7 16 T cells expressing particular y and 5 chain V regions
arise in an ordered sequence early in life. 273
Summary. 275
Interaction with self antigens selects some lymphocytes
for survival but eliminates others. 275
7 17 Immature B cells that bind self antigens undergo
further receptor rearrangement, die, or are inactivated. 276
7 18 The MHC type of the thymic stroma selects a repertoire
of mature T cells that can recognize foreign antigens
presented by the same MHC type. 280
7 19 Only thymocytes whose receptors interact with self MHC:
self peptide complexes can survive and mature. 282
7 20 Positive selection acts on a repertoire of receptors with
inherent specificity for MHC molecules. 283
7 21 Positive selection coordinates the expression of CD4 or
CD8 with the specificity of the T cell receptor and the
potential effector functions of the T cell. 283
7 22 Thymic cortical epithelial cells mediate positive selection
of developing thymocytes. 285
7 23 T cells that react strongly with ubiquitous self antigens
are deleted in the thymus. 287
7 24 Negative selection is driven most efficiently by bone
marrow derived antigen presenting cells. 289
7 25 The specificity and/or the strength of signals for negative
and positive selection must differ. 290
Summary. 292
Survival and maturation of lymphocytes in peripheral
lymphoid tissues. 293
7 26 Lymphocytes are found in particular locations in peripheral
lymphoid tissues. 293
7 27 The development and organization of peripheral lymphoid
tissues is controlled by tumor necrosis factor family
molecules, and the homing of lymphocytes is mediated
by chemokines. 295
7 28 The further development and homeostasis of peripheral
lymphocytes is determined via cytokines and by signals
that lymphocytes continually receive through their antigen
receptors. 297
7 29 Lymphocytes that encounter sufficient quantities of self
antigens for the first time in the periphery are eliminated
or inactivated. 298
7 30 Most immature B cells arriving in the spleen are short lived
and require cytokines and positive signals through the B cell
receptor for maturation and survival. 299
7 31 The specificity of the B cell receptor is important in
determining the differentiation and survival of B cells
in the periphery. 300
7 32 The life span of T cells in the periphery is determined
by cytokines as well as ongoing contact with self peptide:
self MHC complexes similar to those that initially selected
them. 303
7 33 B cell tumors often occupy the same site as their normal
counterparts. 304
7 34 A range of tumors of immune system cells throws light
on different stages of T cell development. 306
7 35 Malignant lymphocyte tumors frequently carry chromosomal
translocations that join immunoglobulin loci to genes that
regulate cell growth. 307
Summary. 308
Summary to Chapter 7. 309
Part IVI THE ADAPTIVE IMMUNE
1 RESPONSE
Chapter 8 T Cell Mediated Immunity 319
The production of armed effector T cells. 321
8 1 T cell responses are initiated in peripheral lymphoid organs
by activated antigen presenting cells. 321
8 2 Naive T cells sample the MHC:peptide complexes on the
surface of antigen presenting cells as they migrate through
peripheral lymphoid tissue. 323
8 3 Lymphocyte migration, activation, and effector function
depend on cell cell interactions mediated by cell adhesion
molecules. 324
8 4 The initial interaction of T cells with antigen presenting cells
is mediated by cell adhesion molecules. 327
8 5 Both specific antigen and co stimulatory signals provided
by the same antigen presenting cell are required for the
clonal expansion of naive T cells. 328
8 6 Dendritic cells specialize in ingesting antigen and activating
naive T cells. 331
8 7 Macrophages are scavenger cells that can be induced by
pathogens to present foreign antigens to naive T cells. 334
8 8 B cells are highly efficient at presenting antigens that bind
to their surface immunoglobulin. 335
8 9 Activated T cells synthesize the T cell growth factor
interieukin 2 and its receptor. 337
8 10 The co stimulatory signal is necessary for the synthesis
and secretion of IL 2. 338
8 11 Antigen recognition in the absence of co stimulation leads
to the inactivation of peripheral T cells. 338
8 12 Proliferating T cells differentiate into armed effector T cells
that do not require co stimulation to act. 339
8 13 The differentiation of CD4 T cells into TH1 or TH2 cells
determines whether humoral or cell mediated immunity
will predominate. 341
8 14 Naive CD8 T cells can be activated in different ways to
become armed cytotoxic effector cells. 341
Summary. 342
General properties of armed effector T cells. 343
8 15 Effector T cell interactions with target cells are initiated by
antigen nonspecific cell adhesion molecules. 344
8 16 Binding of the T cell receptor complex directs the release of
effector molecules and focuses them on the target cell. 344
8 17 The effector functions of T cells are determined by the
array of effector molecules that they produce. 346
8 18 Cytokines can act locally or at a distance. 347
8 19 Cytokines and their receptors fall into distinct families of
structurally related proteins. 349
8 20 The TNF family of cytokines are trimeric proteins that are
usually associated with the cell surface. 350
Summary. 351
T cell mediated cytotoxicity. 351
8 21 Cytotoxic T cells can induce target cells to undergo
programmed cell death. 352
8 22 Cytotoxic effector proteins that trigger apoptosis are
contained in the granules of CD8 cytotoxic T cells. 353
8 23 Activated CD8 T cells and some CD4 effector T cells
express Fas ligand, which can also activate apoptosis. 355
8 24 Cytotoxic T cells are selective and serial killers of
targets expressing specific antigen. 355
8 25 Cytotoxic T cells also act by releasing cytokines. 356
Summary. 356
Macrophage activation by armed CD4 TH1 cells. 357
8 26 Armed Th1 cells have a central role in macrophage
activation. 357
8 27 The production of cytokines and membrane associated
molecules by armed CD4 TH1 cells requires new RNA
and protein synthesis. 358
8 28 Activation of macrophages by armed Th1 cells promotes
microbial killing and must be tightly regulated to avoid
tissue damage. 358
8 29 Th1 cells coordinate the host response to intracellular
pathogens. 359
Summary. 361
Summary to Chapter 8. 361
Chapter 9 The Humoral Immune Response 367
B cell activation by armed helper T cells. 369
9 1 The humoral immune response is initiated when B cells
that bind antigen are signaled by helper T cells or by
certain microbial antigens alone. 369
9 2 Armed helper T cells activate B cells that recognize the
same antigen. 370
9 3 Antigenic peptides bound to self MHC class II molecules
trigger armed helper T cells to make membrane bound
and secreted molecules that can activate a B cell. 372
9 4 Isotype switching in thymus dependent responses requires
expression of CD40 ligand by the helper T cell and is
directed by cytokines. 373
9 5 Antigen binding B cells are trapped in the T cell zone of
secondary lymphoid tissues and are activated by encounter
with armed helper T cells. 375
9 6 The second phase of the primary B cell immune response
occurs when activated B cells migrate to follicles and
proliferate to form germinal centers. 377
9 7 Germinal center B cells undergo V region somatic
hypermutation, and cells with mutations that improve
affinity for antigen are selected. 379
9 8 Ligation of the B cell receptor and CD40, together with
direct contact with T cells, are all required to sustain
germinal center B cells. 382
9 9 Surviving germinal center B cells differentiate into either
plasma cells or memory cells. 383
9 10 B cell responses to bacterial antigens with intrinsic ability
to activate B cells do not require T cell help. 383
9 11 B cell responses to bacterial polysaccharides do not
require peptide specific T cell help. 385
Summary. 387
The distribution and functions of immunoglobulin
isotypes. 387
9 12 Antibodies of different isotype operate in distinct places
and have distinct effector functions. 388
9 13 Transport proteins that bind to the Fc regions of antibodies
carry particular isotypes across epithelial barriers. 389
9 14 High affinity IgG and IgA antibodies can neutralize bacterial
toxins. 392
9 15 High affinity IgG and IgA antibodies can inhibit the infectivity
of viruses. 393
9 16 Antibodies can block the adherence of bacteria to host cells. 394
9 17 Antibody:antigen complexes activate the classical pathway
of complement by binding to C1q. 395
9 18 Complement receptors are important in the removal of
immune complexes from the circulation. 396
Summary. 397
The destruction of antibody coated pathogens via Fc
receptors. 398
9 19 The Fc receptors of accessory cells are signaling receptors
specific for immunoglobulins of different isotypes. 398
9 20 Fc receptors on phagocytes are activated by antibodies
bound to the surface of pathogens and enable the phag¬
ocytes to ingest and destroy pathogens. 399
9 21 Fc receptors activate NK cells to destroy antibody coated
targets. 401
9 22 Mast cells, basophils, and activated eosinophils bind IgE
antibody via the high affinity Fee receptor. 402
9 23 IgE mediated activation of accessory cells has an important
role in resistance to parasite infection. 403
Summary. 404
Summary to Chapter 9. 405
Chapter 10 Adaptive Immunity to Infection 409
Infectious agents and how they cause disease. 410
10 1 The course of an infection can be divided into several
distinct phases. 410
10 2 Infectious diseases are caused by diverse living agents that
replicate in their hosts. 412
Summary. 416
The course of the adaptive response to infection. 416
10 3 The nonspecific responses of innate immunity are necessary
for an adaptive immune response to be initiated. 417
10 4 An adaptive immune response is initiated when circulating
T cells encounter their corresponding antigen in draining
lymphoid tissues and become activated. 418
10 5 Cytokines made in the early phases of an infection influence
the functional differentiation of CD4 T cells. 420
10 6 Distinct subsets of T cells can regulate the growth and
effector functions of other T cell subsets. 423
10 7 The nature and amount of antigenic peptide can also affect
the differentiation of CD4 T cells. 424
10 8 Armed effector T cells are guided to sites of infection by
chemokines and newly expressed adhesion molecules. 425
10 9 Antibody responses develop in lymphoid tissues under the
direction of armed helper T cells. 427
10 10 Antibody responses are sustained in medullary cords and
bone marrow. 428
10 11 The effector mechanisms used to clear an infection depend
on the infectious agent. 429
10 12 Resolution of an infection is accompanied by the death
of most of the effector cells and the generation of memory
cells. 431
Summary. 431
The mucosal immune system. 432
10 13 Mucosa associated lymphoid tissue is located in
anatomically defined microcompartments throughout
the gut. 433
10 14 The trafficking of lymphocytes within different compartments
of the immune system is controlled by tissue specific
adhesion and chemokine interactions. 434
10 15 The mucosal immune system contains a distinctive
repertoire of lymphocytes. 436
10 16 Secretory IgA is the antibody isotype associated with the
mucosal immune system. 438
10 17 Most antigens presented to the mucosal immune system
induce tolerance. 439
10 18 The mucosal immune system can mount an immune
response to the normal bacterial flora of the gut. 439
10 19 Enteric pathogens cause a local inflammatory response
and the development of protective immunity. 440
10 20 Infection by Helicobacter pylori causes a chronic
inflammatory response, which can cause peptic ulcers,
carcinoma of the stomach, and unusual lymphoid tumors. 443
10 21 In the absence of inflammatory stimuli, the normal response
of the mucosal immune system to foreign antigens is
tolerance. 444
Summary. 445
Immunological memory. 446
10 22 Immunological memory is long lived after infection or
vaccination. 446
10 23 Both clonal expansion and clonal differentiation contribute
to immunological memory in B cells. 447
10 24 Repeated immunization leads to increasing affinity of
antibody owing to somatic hypermutation and selection
by antigen in germinal centers. 449
10 25 Memory T cells are increased in frequency and have distinct
activation requirements and cell surface proteins that
distinguish them from armed effector T cells. 450
10 26 In immune individuals, secondary and subsequent
responses are mediated mainly by memory lymphocytes. 451
Summary. 454
Summary to Chapter 10. 454
PartVl THE IMMUNE SYSTEM IN
HEALTH AND DISEASE
Chapter 11 Failures of Host Defense Mechanisms 461
Pathogens have evolved various means of evading or
subverting normal host defenses. 462
11 1 Antigenic variation allows pathogens to escape from
immunity. 462
11 2 Some viruses persist in vivo by ceasing to replicate until
immunity wanes. 465
11 3 Some pathogens resist destruction by host defense
mechanisms or exploit them for their own purposes. 466
11 4 Immunosuppression or inappropriate immune responses
can contribute to persistent disease. 468
11 5 Immune responses can contribute directly to pathogenesis. 470
Summary. 470
Immunodeficiency diseases. 470
11 6 A history of repeated infections suggests a diagnosis of
immunodeficiency. 471
11 7 Inherited immunodeficiency diseases are caused by
recessive gene defects. 472
11 8 The main effect of low levels of antibody is an inability to
clear extracellular bacteria. 474
11 9 T cell defects can also result in low antibody levels. 476
11 10 Defects in complement components cause defective humoral
immune function. 478
11 11 Defects in phagocytic cells permit widespread bacterial
infections. 479
11 12 Defects in T cell function result in severe combined
immunodeficiencies. 480
11 13 Defective T cell signaling, cytokine production, or cytokine
action can cause immunodeficiency. 483
11 14 The normal pathways for host defense against intracellular
bacteria are illustrated by genetic deficiencies of IFN y and
IL 12 and their receptors. 485
11 15 X linked lymphoproliferative syndrome is associated with
fatal infection by Epstein Barr virus and with the
development of lymphomas. 486
11 16 Genetic abnormalities in the secretory cytotoxic pathway of
lymphocytes cause uncontrolled lymphoproliferation and
inflammatory responses to viral infections. 487
11 17 Bone marrow transplantation or gene therapy can be useful
to correct genetic defects. 488
11 18 Secondary immunodeficiencies are major predisposing
causes of infection and death. 489
Summary. 490
Acquired immune deficiency syndrome. 491
11 19 Most individuals infected with HIV progress over time
to AIDS. 492
11 20 HIV is a retrovirus that infects CD4 T cells, dendritic cells,
and macrophages. 494
11 21 Genetic deficiency of the macrophage chemokine
co receptor for HIV confers resistance to HIV infection
in vivo. 496
11 22 HIV RNA is transcribed by viral reverse transcriptase
into DNA that integrates into the host cell genome. 497
11 23 Transcription of the HIV provirus depends on host cell
transcription factors induced upon the activation of infected
T cells. 499
11 24 Drugs that block HIV replication lead to a rapid decrease
in titer of infectious virus and an increase in CD4 T cells. 500
11 25 HIV accumulates many mutations in the course of infection
in a single individual and drug treatment is soon followed
by the outgrowth of drug resistant variants of the virus. 501
11 26 Lymphoid tissue is the major reservoir of HIV infection. 502
11 27 An immune response controls but does not eliminate HIV. 503
11 28 HIV infection leads to low levels of CD4 T cells, increased
susceptibility to opportunistic infection, and eventually
to death. 505
11 29 Vaccination against HIV is an attractive solution but poses
many difficulties. 506
11 30 Prevention and education are one way in which the spread
of HIV and AIDS can be controlled. 507
Summary. 508
Summary to Chapter 11. 508
Chapter 12 Allergy and Hypersensitivity 517
Sensitization and the production of IgE. 519
12 1 Allergens are often delivered transmucosally at low dose,
a route that favors IgE production. 519
12 2 Enzymes are frequent triggers of allergy. 520
12 3 Class switching to IgE in B lymphocytes is favored by
specific signals. 521
12 4 Both genetic and environmental factors contribute to the
development of IgE mediated allergy. 523
Summary. 527
Effector mechanisms in allergic reactions. 527
12 5 Most IgE is cell bound and engages effector mechanisms
of the immune system by different pathways from other
antibody isotypes. 528
12 6 Mast cells reside in tissues and orchestrate allergic
reactions. 529
12 7 Eosinophils are normally under tight control to prevent
inappropriate toxic responses. 530
12 8 Eosinophils and basophils cause inflammation and tissue
damage in allergic reactions. 532
12 9 Allergic reactions can be divided into immediate and
late phase responses. 533
12 10 The clinical effects of allergic reactions vary according to
the site of mast cell activation. 534
12 11 Allergen inhalation is associated with the development of
rhinitis and asthma. 535
12 12 Skin allergy is manifest as urticaria or chronic eczema. 538
12 13 Allergy to foods causes symptoms limited to the gut and
systemic reactions. 539
12 14 Allergy can be treated by inhibiting either IgE production
or the effector pathways activated by cross linking of
cell surface IgE. 539
Summary. 541
Hypersensitivity diseases. 542
12 15 Innocuous antigens can cause type II hypersensitivity
reactions in susceptible individuals by binding to the
surfaces of circulating blood cells. 542
12 16 Systemic disease caused by immune complex formation
can follow the administration of large quantities of poorly
catabolized antigens. 542
12 17 Delayed type hypersensitivity reactions are mediated by
TH1 cells and CD8 cytotoxic T cells. 544
12 18 Mutation or genetic variation in the molecular regulators of
inflammation can cause hypersensitive inflammatory
responses resulting in autoinflammatory disease . 547
Summary. 550
Summary to Chapter 12. 550
Chapter 13 Autoimmunity and Transplantation 557
The nature of immune responses to self. 557
13 1 A critical function of the immune system is to discriminate
self from nonself. 558
13 2 Specific adaptive immune responses to self antigens can
cause autoimmune disease. 559
13 3 Autoimmune diseases can be classified into clusters that
are typically either organ specific or systemic. 560
13 4 Multiple limbs of the immune system are typically recruited
in autoimmune disease. 561
13 5 Initial loss of tolerance and autoimmunity may evolve to a
chronic disease state because of positive feedback from
inflammation as well as the inability to clear most self
antigens. 564
Summary. 566
Multiple tolerance mechanisms normally prevent
autoimmunity. 566
13 6 Some degree of autoimmunity is the evolutionary price of
being able to make effective responses against pathogens. 567
13 7 Central deletion or inactivation of newly formed lymphocytes
is the first checkpoint of self tolerance. 567
13 8 Lymphocytes that bind self antigens with relatively low affinity
usually ignore them but in some circumstances become
activated. 569
13 9 Antigens in immunologically privileged sites do not induce
immune attack but can serve as targets. 570
13 10 Autoreactive T cells that express particular cytokines may
be nonpathogenic or suppress pathogenic lymphocytes. 572
13 11 Autoimmune responses can be controlled at various stages
by regulatory T cells. 572
13 12 CD4 CD25 T cells are a unique subset of cells that arise in
the thymus in response to relatively strong recognition of
self antigen. 573
13 13 The mechanisms of regulation are varied and can include
cytokine mediated inhibition, contact dependent regulation,
and cell killing. 574
13 14 Other types of regulatory cell also exist. 575
13 15 Immune responses have natural brakes that tend to limit
damage even when autoimmune cells are activated. 576
Summary. 576
The genetic and environmental basis of autoimmunity. 578
13 16 Autoimmune diseases have a strong genetic as well as
environmental component. 578
13 17 Several approaches have given us insight into the genetic
basis of autoimmunity. 579
13 18 Genes that predispose to autoimmunity fall into categories
that affect one or more of the layers of tolerance. 580
13 19 MHC genes have an important role in controlling suscept¬
ibility to autoimmune disease. 582
13 20 Molecular pathways promoting autoimmunity are potential
targets for the therapy of autoimmune disease. 584
13 21 Drugs and toxins can cause autoimmune syndromes. 585
13 22 Infection can lead to autoimmune disease. 585
13 23 Cross reactivity between self molecules and foreign mol¬
ecules on pathogens can lead to anti self responses and
autoimmune disease. 586
13 24 Random events may be required for the initiation of
autoimmunity. 587
Summary. 588
Mechanisms of pathogenesis in autoimmunity. 588
13 25 Antibody and T cells can cause tissue damage in auto¬
immune disease. 589
13 26 Autoantibodies against blood cells promote their
destruction. 590
13 27 The fixation of sublytic doses of complement to cells in
tissues stimulates a powerful inflammatory response. 591
13 28 Autoantibodies against receptors cause disease by
stimulating or blocking receptor function. 592
13 29 Autoantibodies against extracellular antigens cause
inflammatory injury by mechanisms akin to type II and
type III hypersensitivity reactions. 593
13 30 T cells specific for self antigens can cause direct tissue
injury and have a role in sustained autoantibody responses. 595
Summary. 595
Responses to alloantigens and transplant rejection. 596
13 31 Graft rejection is an immunological response mediated
primarily by T cells. 597
13 32 Matching donor and recipient at the MHC improves the
outcome of transplantation. 598
13 33 In MHC identical grafts, rejection is caused by peptides
from other alloantigens bound to graft MHC molecules. 599
13 34 There are two ways of presenting alloantigens on the
transplant to the recipient s T lymphocytes. 600
13 35 Antibodies reacting with endothelium cause hyperacute
graft rejection. 602
13 36 Chronic organ rejection is caused by inflammatory vascular
injury to the graft. 602
13 37 A variety of organs are transplanted routinely in clinical
medicine. 603
13 38 The converse of graft rejection is graft versus host disease. 604
13 39 The fetus is an allograft that is tolerated repeatedly. 606
Summary. 607
Summary to Chapter 13. 607
Chapter 14 Manipulation of the Immune Response 613
Extrinsic regulation of unwanted immune responses. 614
14 1 Corticosteroids are powerful anti inflammatory drugs that
alter the transcription of many genes. 614
14 2 Cytotoxic drugs cause immunosuppression by killing
dividing cells and have serious side effects. 615
14 3 Cyclosporin A, tacrolimus (FK506), and rapamycin
(sirolimus) are powerful immunosuppressive agents that
interfere with T cell signaling. 616
14 4 Immunosuppressive drugs are valuable probes of intra
cellular signaling pathways in lymphocytes. 617
14 5 Antibodies against cell surface molecules have been used
to remove specific lymphocyte subsets or to inhibit cell
function. 619
14 6 Antibodies can be engineered to reduce their immuno
genicity in humans. 619
14 7 Monoclonal antibodies can be used to inhibit allograft
rejection. 620
14 8 Biological agents can be used to alleviate and suppress
autoimmune disease. 622
14 9 Depletion or inhibition of autoreactive lymphocytes can treat
autoimmune disease. 624
14 10 Interference with co stimulatory pathways for the activation
of lymphocytes could be a treatment for autoimmune
disease. 626
14 11 Modulation of the cytokines expressed by T lymphocytes
can inhibit autoimmune disease. 626
14 12 Controlled administration of antigen can be used to
manipulate the nature of an antigen specific response. 628
Summary. 629
Using the immune response to attack tumors. 630
14 13 The development of transplantable tumors in mice led to
the discovery that mice could mount a protective immune
response against tumors. 630
14 14 T lymphocytes can recognize specific antigens on human
tumors. 631
14 15 Tumors can escape rejection in many ways. 635
14 16 Monoclonal antibodies against tumor antigens, alone or
linked to toxins, can control tumor growth. 638
14 17 Enhancing the immunogenicity of tumors holds promise
for cancer therapy. 640
Summary. 642
Manipulating the immune response to fight infection. 642
14 18 There are several requirements for an effective vaccine. 644
14 19 The history of vaccination against Bordetella pertussis
illustrates the importance of developing an effective vaccine
that is perceived to be safe. 645
14 20 Conjugate vaccines have been developed as a result of
understanding how T and B cells collaborate in an immune
response. 646
14 21 The use of adjuvants is another important approach to
enhancing the immunogenicity of vaccines. 647
14 22 Live attenuated viral vaccines are usually more potent than
killed vaccines and can be made safer by using recomb
inant DNA technology. 649
14 23 Live attenuated bacterial vaccines can be developed by
selecting nonpathogenic or disabled mutants. 650
14 24 Attenuated microorganisms can serve as vectors for
vaccination against many pathogens. 650
14 25 Synthetic peptides of protective antigens can elicit
protective immunity. 651
14 26 The route of vaccination is an important determinant of
success. 653
14 27 Protective immunity can be induced by injecting DNA
encoding microbial antigens and human cytokines into
muscle. 653
14 28 The effectiveness of a vaccine can be enhanced by
targeting it to sites of antigen presentation. 654
14 29 An important question is whether vaccination can be used
therapeutically to control existing chronic infections. 655
14 30 Modulation of the immune system might be used to inhibit
immunopathological responses to infectious agents. 656
Summary. 656
Summary to Chapter 14. 657
Part VII THE ORIGINS OF IMMUNE
1 RESPONSES
Chapter 15 Evolution of the Immune System 665
Evolution of the innate immune system. 667
15 1 Antimicrobial peptides are likely to be the most ancient
immune defenses. 667
15 2 Toll like receptors may represent the most primitive
pathogen recognition system. 668
15 3 A second recognition system in Drosophila homologous
to the mammalian tumor necrosis factor receptor pathway
provides protection from Gram negative bacteria. 670
15 4 An ancestral complement system opsonizes pathogens for
uptake by phagocytic cells. 671
15 5 The lectin pathway of complement activation evolved in
invertebrates. 672
Summary. 673
Evolution of the adaptive immune response. 673
15 6 Adaptive immunity appeared abruptly in the cartilaginous
fish. 674
15 7 The target of the transposon is likely to have been a gene
encoding a cell surface receptor containing an immuno
globulin like V domain. 676
15 8 Different species generate immunoglobulin diversity in
different ways. 676
15 9 Both a:P and y:8 T cell receptors are present in cartila¬
ginous fish. 678
15 10 MHC class I and class II molecules are also first found
in the cartilaginous fishes. 678
15 11 Are adaptive immune systems dependent on the emerg¬
ence of the jaw? 679
Summary. 680
Summary to Chapter 15. 680
Appendix I Immunologists Toolbox 683
Immunization. 683
A 1 Haptens. 684
A 2 Routes of immunization. 686
A 3 Effects of antigen dose. 686
A 4 Adjuvants. 686
The detection, measurement, and characterization of
antibodies and their use as research and diagnostic
tools. 688
A 5 Affinity chromatography. 689
A 6 Radioimmunoassay (RIA), enzyme linked immunosorbent
assay (ELISA), and competitive inhibition assay. 689
A 7 Hemagglutination and blood typing. 691
A 8 Precipitin reaction. 692
A 9 Equilibrium dialysis: measurement of antibody affinity and
avidity. 693
A 10 Anti immunoglobulin antibodies. 694
A 11 Coombs tests and the detection of Rhesus incompatibility. 695
A 12 Monoclonal antibodies. 696
A 13 Phage display libraries for antibody V region production. 697
A 14 Immunofluorescence microscopy. 698
A 15 Immunoelectron microscopy. 700
A 16 Immunohistochemistry. 701
A 17 Immunoprecipitation and co immunoprecipitation. 701
A 18 Immunoblotting (Western blotting). 702
A 19 Use of antibodies in the isolation and identification of genes
and their products. 703
Isolation of lymphocytes. 705
A 20 Isolation of peripheral blood lymphocytes by Ficoll Hypaque™
gradient. 705
A 21 Isolation of lymphocytes from tissues other than blood. 705
A 22 Flow cytometry and FACS analysis. 706
A 23 Lymphocyte isolation using antibody coated magnetic
beads. 708
A 24 Isolation of homogeneous T cell lines. 708
Characterization of lymphocyte specificity, frequency,
and function. 709
A 25 Limiting dilution culture. 710
A 26 ELISPOT assays. 711
A 27 Identification of functional subsets of T cells by staining for
cytokines. 712
A 28 Identification of T cell receptor specificity using MHC:
peptide tetramers. 713
A 29 Assessing the diversity of the T cell repertoire by
spectratyping. 714
A 30 Biosensor assays for measuring the rates of association
and disassociation of antigen receptors for their ligands. 714
A 31 Stimulation of lymphocyte proliferation by treatment with
polyclonal mitogens or specific antigen. 716
A 32 Measurements of apoptosis by the TUNEL assay. 717
A 33 Assays for cytotoxic T cells. 717
A 34 Assays for CD4 T cells. 717
A 35 DNA microarrays. 718
Detection of immunity in vivo. 720
A 36 Assessment of protective immunity. 720
A 37 Transfer of protective immunity. 720
A 38 The tuberculin test. 721
A 39 Testing for allergic responses. 721
A 40 Assessment of immune responses and immunological
competence in humans. 721
A 41 The Arthus reaction. 723
Manipulation of the immune system. 723
A 42 Adoptive transfer of lymphocytes. 723
A 43 Hematopoietic stem cell transfers. 724
A 44 In vivo depletion of T cells. 724
A 45 In vivo depletion of B cells. 724
A 46 Transgenic mice. 725
A 47 Gene knockout by targeted disruption. 726
Appendix II CD antigens 731
Appendix III Cytokines and their receptors 747
Appendix IV Chemokines and their receptors 750
Appendix V Immunological constants 751
Biographies 752
Glossary 753
Index 778
|
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| discipline | Biologie Chemie Medizin |
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| indexdate | 2024-07-09T19:22:59Z |
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| owner_facet | DE-20 DE-29 DE-355 DE-BY-UBR DE-M49 DE-BY-TUM DE-91G DE-BY-TUM DE-526 DE-11 |
| physical | XXIII, 823 S. zahlr. Ill., graph. Darst. 1 CD-ROM (12 cm) |
| publishDate | 2005 |
| publishDateSearch | 2005 |
| publishDateSort | 2005 |
| publisher | Garland Science |
| record_format | marc |
| spelling | Immunobiology the immune system in health and disease Charles A. Janeway ... Immunobiology interactive 6. ed. New York, NY [u.a.] Garland Science 2005 XXIII, 823 S. zahlr. Ill., graph. Darst. 1 CD-ROM (12 cm) txt rdacontent n rdamedia nc rdacarrier CD-ROM u.d.T.: Immunobiology interactive. - 7. Aufl. u.d.T.: Murphy, Kenneth: Janeway's immunobiology CD-ROM Immune System Immunity Immunology Immunbiologie (DE-588)4072743-9 gnd rswk-swf CD-ROM (DE-588)4139307-7 gnd rswk-swf Immunologie (DE-588)4026637-0 gnd rswk-swf (DE-588)4123623-3 Lehrbuch gnd-content Immunologie (DE-588)4026637-0 s DE-604 Immunbiologie (DE-588)4072743-9 s CD-ROM (DE-588)4139307-7 s 1\p DE-604 Janeway, Charles A. Jr. 1943-2003 Sonstige (DE-588)123088178 oth HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010734186&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis 1\p cgwrk 20201028 DE-101 https://d-nb.info/provenance/plan#cgwrk |
| spellingShingle | Immunobiology the immune system in health and disease CD-ROM Immune System Immunity Immunology Immunbiologie (DE-588)4072743-9 gnd CD-ROM (DE-588)4139307-7 gnd Immunologie (DE-588)4026637-0 gnd |
| subject_GND | (DE-588)4072743-9 (DE-588)4139307-7 (DE-588)4026637-0 (DE-588)4123623-3 |
| title | Immunobiology the immune system in health and disease |
| title_alt | Immunobiology interactive |
| title_auth | Immunobiology the immune system in health and disease |
| title_exact_search | Immunobiology the immune system in health and disease |
| title_full | Immunobiology the immune system in health and disease Charles A. Janeway ... |
| title_fullStr | Immunobiology the immune system in health and disease Charles A. Janeway ... |
| title_full_unstemmed | Immunobiology the immune system in health and disease Charles A. Janeway ... |
| title_short | Immunobiology |
| title_sort | immunobiology the immune system in health and disease |
| title_sub | the immune system in health and disease |
| topic | CD-ROM Immune System Immunity Immunology Immunbiologie (DE-588)4072743-9 gnd CD-ROM (DE-588)4139307-7 gnd Immunologie (DE-588)4026637-0 gnd |
| topic_facet | CD-ROM Immune System Immunity Immunology Immunbiologie Immunologie Lehrbuch |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=010734186&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
| work_keys_str_mv | AT janewaycharlesa immunobiologytheimmunesysteminhealthanddisease AT janewaycharlesa immunobiologyinteractive |