The immune system:
Gespeichert in:
| 1. Verfasser: | |
|---|---|
| Format: | Buch |
| Sprache: | English |
| Veröffentlicht: |
London [u.a.]
Garland Science
c2009
|
| Ausgabe: | 3. ed. |
| Schlagworte: | |
| Online-Zugang: | Inhaltsverzeichnis |
| Beschreibung: | XVII, 506, [83] S. zahlr. Ill., graph. Darst. |
| ISBN: | 9780815341468 |
Internformat
MARC
| LEADER | 00000nam a2200000zc 4500 | ||
|---|---|---|---|
| 001 | BV035368052 | ||
| 003 | DE-604 | ||
| 005 | 20090512 | ||
| 007 | t | ||
| 008 | 090313s2009 xxuad|| |||| 00||| eng d | ||
| 010 | |a 2008034011 | ||
| 020 | |a 9780815341468 |9 978-0-8153-4146-8 | ||
| 035 | |a (OCoLC)240989634 | ||
| 035 | |a (DE-599)BVBBV035368052 | ||
| 040 | |a DE-604 |b ger |e aacr | ||
| 041 | 0 | |a eng | |
| 044 | |a xxu |c US | ||
| 049 | |a DE-29 | ||
| 050 | 0 | |a QR181 | |
| 082 | 0 | |a 616.07/9 | |
| 084 | |a WF 9800 |0 (DE-625)148471: |2 rvk | ||
| 100 | 1 | |a Parham, Peter |d 1950- |e Verfasser |0 (DE-588)136599443 |4 aut | |
| 245 | 1 | 0 | |a The immune system |c Peter Parham |
| 250 | |a 3. ed. | ||
| 264 | 1 | |a London [u.a.] |b Garland Science |c c2009 | |
| 300 | |a XVII, 506, [83] S. |b zahlr. Ill., graph. Darst. | ||
| 336 | |b txt |2 rdacontent | ||
| 337 | |b n |2 rdamedia | ||
| 338 | |b nc |2 rdacarrier | ||
| 650 | 2 | |a Immunité | |
| 650 | 2 | |a Système immunitaire | |
| 650 | 4 | |a Immune system | |
| 650 | 4 | |a Immunopathology | |
| 650 | 4 | |a Immune System | |
| 650 | 4 | |a Immunity | |
| 650 | 0 | 7 | |a Immunsystem |0 (DE-588)4026643-6 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Immunbiologie |0 (DE-588)4072743-9 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Immunreaktion |0 (DE-588)4133841-8 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Krebs |g Medizin |0 (DE-588)4073781-0 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Autoaggressionskrankheit |0 (DE-588)4003935-3 |2 gnd |9 rswk-swf |
| 650 | 0 | 7 | |a Immunpathologie |0 (DE-588)4014133-0 |2 gnd |9 rswk-swf |
| 689 | 0 | 0 | |a Immunsystem |0 (DE-588)4026643-6 |D s |
| 689 | 0 | 1 | |a Immunreaktion |0 (DE-588)4133841-8 |D s |
| 689 | 0 | 2 | |a Krebs |g Medizin |0 (DE-588)4073781-0 |D s |
| 689 | 0 | 3 | |a Autoaggressionskrankheit |0 (DE-588)4003935-3 |D s |
| 689 | 0 | |8 1\p |5 DE-604 | |
| 689 | 1 | 0 | |a Immunsystem |0 (DE-588)4026643-6 |D s |
| 689 | 1 | 1 | |a Immunpathologie |0 (DE-588)4014133-0 |D s |
| 689 | 1 | 2 | |a Immunbiologie |0 (DE-588)4072743-9 |D s |
| 689 | 1 | |8 2\p |5 DE-604 | |
| 856 | 4 | 2 | |m HBZ Datenaustausch |q application/pdf |u http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=017171988&sequence=000004&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |3 Inhaltsverzeichnis |
| 999 | |a oai:aleph.bib-bvb.de:BVB01-017171988 | ||
| 883 | 1 | |8 1\p |a cgwrk |d 20201028 |q DE-101 |u https://d-nb.info/provenance/plan#cgwrk | |
| 883 | 1 | |8 2\p |a cgwrk |d 20201028 |q DE-101 |u https://d-nb.info/provenance/plan#cgwrk | |
Datensatz im Suchindex
| _version_ | 1804138695061667840 |
|---|---|
| adam_text | Titel: The immune system
Autor: Parham, Peter
Jahr: 2009
Contents
Chapter 1 Elements of the Immune System and their Roles
in Defense 1
Chapter 2 Innate Immunity 31
Chapter 3 Principles of Adaptive Immunity 71
Chapter 4 Antibody Structure and the Generation of B-Cell Diversity 95
Chapter 5 Antigen Recognition by T Lymphocytes 125
Chapter 6 The Development of B Lymphocytes 159
Chapter 7 The Development of T Lymphocytes 187
Chapter 8 T Cell-Mediated Immunity 211
Chapter 9 Immunity Mediated by B Cells and Antibodies 249
Chapter 10 The Body s Defenses Against Infection 289
Chapter 11 Failures of the Body s Defenses 329
Chapter 12 Over-reactions of the Immune System 365
Chapter 13 Disruption of Healthy Tissue by the Immune Response 403
Chapter 14 Vaccination to Prevent Infectious Disease 437
Chapter 15 Transplantation of Tissues and Organs 455
Chapter 16 Cancer and Its Interactions with the Immune System 489
Answers to Questions A: 1
Glossary G:l
Figure Acknowledgments F: 1
Index 1:1
Detailed Contents
Chapter 1
Elements of the Immune System and their Roles
in Defense 1
1-1 Numerous commensal microorganisms
inhabit healthy human bodies 2
1 -2 Pathogens are infectious organisms that
cause disease 3
1-3 The skin and mucosal surfaces form barriers
against infection 5
1-4 The innate immune response causes
inflammation at sites of infection 8
1-5 The adaptive immune response adds to an
ongoing innate immune response 10
1-6 Adaptive immunity is better understood than
innate immunity 12
1 - 7 Immune system cells with different functions
all derive from hematopoietic stem cells 12
1-8 Most lymphocytes are present in specialized
lymphoid tissues 17
1-9 Adaptive immunity is initiated in secondary
lymphoid tissues 19
1-10 The spleen provides adaptive immunity to
blood infections 21
1-11 Most secondary lymphoid tissue is associated
with the gut 22
1-12 Adaptive immune responses generally give
rise to long-lived immunological memory
and protective immunity 23
1-13 The immune system can be compromised
by inherited immunodeficiencies or by the
actions of certain pathogens 25
Summary to Chapter 1 26
Questions 27
Chapter 2
Innate Immunity 31
2-1 A variety of defense mechanisms have evolved
to eliminate the different types of pathogen 31
2-2 Complement is a system of plasma proteins
that marks pathogens for destruction 33
2-3 At the start of an infection, complement
activation proceeds by the alternative
pathway 35
2-4 Regulatory proteins determine the extent
and site of C3b deposition 36
2-5 Phagocytosis by macrophages provides a
first line of cellular defense against invading
microorganisms 38
2-6 The terminal complement proteins lyse
pathogens by forming a membrane pore 39
2-7 Small peptides released during complement
activation induce local inflammation 41
2-8 Several classes of plasma protein limit the
spread of infection 42
2-9 Defensins are a family of variable
antimicrobial peptides 43
2-10 Innate immune receptors distinguish features
of microbial structure 44
2-11 Toll-like receptors sense the presence of
infection 45
2-12 Signaling through Toll-like receptors leads
to two different cytokine responses 47
2-13 Activation of resident macrophages induces
inflammation at sites of infection 49
2-14 Neutrophils are dedicated phagocytes that
are summoned to sites of infection 53
2-15 The homing of neutrophils to inflamed tissues
involves altered interactions with vascular
endothelium 54
2-16 Neutrophils are potent killers of pathogens
and are themselves programmed to die 56
2-17 Inflammatory cytokines raise body temperature
and activate hepatocytes to make the acute-
phase response 58
2-18 The lectin pathway of complement activation
is initiated by mannose-binding lectin 60
2-19 C-reactive protein triggers the classical
pathway of complement activation 62
2-20 Type I interferons inhibit viral replication
and activate host defenses 62
2-21 NK cells provide an early defense against
intracellular infections
2-22 NK-cell receptors differ in the ligands they
bind and the signals they generate 66
Summary to Chapter 2 ^
Questions
Chapter 3
Principles of Adaptive Immunity 71
3-1 Innate and adaptive immunity differ in their
strategies for pathogen recognition 71
3-2 Immunoglobulins and T-cell receptors are
the highly variable recognition molecules
of adaptive immunity 72
3-3 The diversity of immunoglobulins and T-cell
receptors is generated by gene
rearrangement 73
3 -4 Clonal selection of B and T lymphocytes is
the guiding principle of the adaptive immune
response 75
3-5 Adaptive immune responses are initiated in
secondary lymphoid tissues by antigen-
bearing dendritic cells and T cells 75
3-6 T-cell receptors recognize degraded fragments
of pathogen proteins 76
3-7 T-cell receptors recognize peptide antigens
bound to human cell-surface molecules 78
3-8 Two classes of MHC molecule present peptide
antigens to two types of T cell 78
3-9 MHC class I molecules present antigens of
intracellular origin to CD8 T cells 80
3-10 MHC class II molecules present antigens of
extracellular origin to CD4 T cells 81
3-11 Effector CD4 T cells help B cells become
antibody-producing plasma cells 81
3-12 Extracellular pathogens and their toxins are
eliminated by antibodies 83
3-13 Antibody quality improves during the course
of an adaptive immune response 85
3-14 Immunological memory is a consequence
of clonal selection 86
3-15 Clonal selection makes T cells and B cells
tolerant of self and responsive to pathogens 87
3-16 Unwanted effects of adaptive immunity cause
autoimmune disease, transplant rejection
and allergy 88
Summary to Chapter 3 90
Questions 91
Chapter 4
Antibody Structure and the Generation of
B-Cell Diversity 95
The structural basis of antibody diversity 96
4-1 Antibodies are composed of polypeptides
with variable and constant regions 96
4-2 Immunoglobulin chains are folded into
compact and stable protein domains 97
4-3 An antigen-binding site is formed from the
hypervariable regions of a heavy-chain
V domain and a light-chain V domain 99
4-4 Antigen-binding sites vary in shape and
physical properties 100
4-5 Monoclonal antibodies are produced from
a clone of antibody-producing cells 102
4-6 Monocolonal antibodies are used as
treatments for a variety of diseases 104
Summary 105
Detailed Contents xi
Generation of immunoglobulin diversity in
B cells before encounter with antigen 105
4-7 The DNA sequence encoding a V region is
assembled from two or three gene segments 106
4-8 Random recombination of gene segments
produces diversity in the antigen-binding
sites of immunoglobulins 106
4-9 Recombination enzymes produce additional
diversity in the antigen-binding site 108
4-10 Developing and naive B cells use alternative
mRNA splicing to make both IgM and IgD 110
4-11 Each B cell produces immunoglobulin of
a single antigen specificity 111
4-12 Immunoglobulin is first made in a membrane-
bound form that is present on the B-cell
surface 111
Summary 112
Diversification of antibodies after B cells
encounter antigen 113
4-13 Secreted antibodies are produced by an
alternative pattern of heavy-chain RNA
processing 113
4-14 Rearranged V-region sequences are further
diversified by somatic hypermutation 114
4-15 Isotype switching produces immunoglobulins
with different C regions but identical antigen
specificities 115
4-16 Antibodies with different C regions have
different effector functions 117
Summary 119
Summary toChapter4 119
Questions 121
Chapter 5
Antigen Recognition by T Lymphocytes 125
T-ceU receptor diversity 126
5-1 The T-cell receptor resembles a membrane-
associated Fab fragment of immunoglobulin 126
5-2 T-cell receptor diversity is generated by gene
rearrangement 127
5-3 The RAG genes were key elements in the
origin of adaptive immunity 129
5-4 Expression of the T-cell receptor on the cell
surface requires association with additional
proteins 129
5-5 A distinct population of T cells expresses a
second class of T-cell receptor with y and
8 chains 130
Summary 131
Antigen processing and presentation 132
5-6 The two classes of MHC molecule present
antigen to CD8 and CD4 T cells, respectively 133
5-7 The two classes of MHC molecule have similar
three-dimensional structures 134
5-8 MHC molecules bind a variety of peptides 135
5-9 MHC class I and class II molecules bind
peptides in different intracellular
compartments 137
5-10 Peptides generated in the cytosol are
transported into the endoplasmic reticulum,
where they bind MHC class I molecules 137
Detailed Contents
5-11 MHC class I molecules bind antigenic peptide
as part of a peptide-loading complex 138
5-12 Peptides presented by MHC class II
molecules are generated in acidified
intracellular vesicles 140
5-13 MHC class II molecules are prevented from
binding peptides in the endoplasmic
reticulum by the invariant chain 140
5-14 The T-cell receptor specifically recognizes
both peptide and MHC molecule 142
5-15 The two classes of MHC molecule are
expressed differentially on cells 143
5-16 Cross-presentation allows extracellular
antigens to be presented by MHC class I 144
Summary 145
The major histocompatibility complex 145
5-17 The diversity of MHC molecules in the human
population is due to multigene families and
genetic polymorphism 146
5-18 The HLA class I and class II genes occupy
different regions of the HLA complex 147
5-19 Other proteins involved in antigen processing
and presentation are encoded in the HLA
class II region 148
5-20 MHC polymorphism affects the binding and
presentation of peptide antigens to T cells 149
5-21 MHC diversity results from selection by
infectious disease 151
5-22 MHC polymorphism triggers T-cell reactions
that can reject transplanted organs 153
Summary 154
Summary to Chapter 5 154
Questions 155
Chapter 6
The Development of B Lymphocytes 159
The development of B cells in the bone
marrow 160
6-1 B-cell development in the bone marrow
proceeds through several stages 160
6-2 B-cell development is stimulated by bone
marrow stromal cells 161
6-3 Pro-B cell rearrangement of the heavy-chain
locus is an inefficient process 162
6-4 The pre-B-cell receptor monitors the quality
of immunoglobulin heavy chains 163
6-5 The pre-B-cell receptor causes allelic exclusion
at the immunoglobulin heavy-chain locus 164
6-6 Rearrangement of the light-chain loci by
pre-B cells is relatively efficient 165
6-7 B cells have to pass two main checkpoints in
their development in the bone marrow 167
6-8 A program of protein expression underlies
the stages of B-cell development 168
6-9 Many B-cell tumors carry chromosomal
translocations that join immunoglobulin
genes to genes that regulate cell growth 171
6-10 B cells expressing the glycoprotein CD5
express a distinctive repertoire of receptors 171
Summary 173
Selection and further development of the
B-cell repertoire 174
6-11 The population of immature B cells is purged
of cells bearing self-reactive B-cell receptors 174
6-12 The antigen receptors of autoreactive immature
B cells can be modified by receptor editing 175
6-13 Immature B cells specific for monovalent self
antigens are made nonresponsive to antigen 176
6-14 Maturation and survival of B cells requires
access to lymphoid follicles 177
6-15 Encounter with antigen leads to the
differentiation of activated B cells into
plasma cells and memory B cells 179
6-16 Different types of B-cell tumor reflect B cells
at different stages of development 180
Summary 182
Summary to Chapter 6 182
Questions 184
Chapter 7
The Development of T Lymphocytes 187
The development of T cells in the thymus 187
7-1 T cells develop in the thymus 188
7-2 Thymocytes commit to the T-cell lineage before
rearranging their T-cell receptor genes 190
7-3 The two lineages of T cells arise from a
common thymocyte progenitor 191
7-4 Gene rearrangement in double-negative
thymocytes leads to assembly of either
a 7:8 receptor or a pre-T-cell receptor 193
7 -5 Thymocytes can make four attempts to
rearrange a P-chain gene 194
7-6 Rearrangement of the a-chain gene occurs
only in pre-T cells 195
7-7 Stages in T-cell development are marked by
changes in gene expression 196
Summary 197
Positive and negative selection of the
T-cell repertoire 198
7-8 T cells that recognize self-MHC molecules
are positively selected in the thymus 199
7-9 Continuing a-chain gene rearrangement
increases the chance for positive selection 200
7-10 Positive selection determines expression of
either the CD4 or the CD8 co-receptor 200
7-11 T cells specific for self antigens are removed
in the thymus by negative selection 202
7-12 Tissue-specific proteins are expressed in the
thymus and participate in negative selection 202
7-13 Regulatory CD4 T cells comprise a distinct
lineage of CD4 T cells 203
7-14 T cells undergo further differentiation in
secondary lymphoid tissues after
encounter with antigen 203
7-15 Most T-cell tumors represent early or late
stages of T-cell development 204
Summary 205
Summary to Chapter 7 205
Questions 207
Chapter 8
T Cell-Mediated Immunity 211
Activation of naive T cells on encounter
with antigen 212
8-1 Dendritic cells carry antigens from sites of
infection to secondary lymphoid tissues 212
8-2 Dendritic cells are adept and versatile at
processing antigens from pathogens 213
8-3 Naive T cells first encounter antigen presented
by dendritic cells in secondary lymphoid
tissues 215
8-4 Homing of naive T cells to secondary lymphoid
tissues is determined by chemokines and
cell-adhesion molecules 216
8-5 Activation of naive T cells requires a co-
stimulatory signal delivered by a professional
antigen-presenting cell 219
8-6 Secondary lymphoid tissues contain three kinds
of professional antigen-presenting cell 220
8-7 When T cells are activated by antigen, signals
from T-cell receptors and co-receptors alter
the pattern of gene transcription 222
8-8 Proliferation and differentiation of activated
T cells are driven by the cytokine
interleukin-2 224
8-9 Antigen recognition by a naive T cell in the
absence of co-stimulation leads to the T cell
becoming nonresponsive 226
8-10 On activation, CD4 T cells acquire distinctive
helper functions 227
8-11 Naive CD8 T cells are activated to become
cytotoxic effector cells in several different
ways 229
Summary 230
The properties and functions of effector
T cells 231
8-12 Effector T-cell responses to infection do not
depend on co-stimulatory signals 231
8-13 Effector T-cell functions are carried out by
cytokines and cytotoxins 232
8-14 Cytotoxic CD8 T cells are selective and serial
killers of target cells at sites of infection 234
8-15 Cytotoxic T cells kill their target cells by
inducing apoptosis 236
8-16 ThI CD4 cells induce macrophages to
become activated 237
8-17 TH1 cells coordinate the host response to
pathogens that live in macrophages 239
8-18 CD4 TH2 cells activate only those B cells that
recognize the same antigen as they do 241
8-19 Regulatory CD4 T cells limit the activities of
effector CD4 and CD8 T cells 242
Summary 243
Summary to Chapter 8 245
Questions 245
Chapter 9
Immunity Mediated by B Cells and Antibodies 249
Antibody production by B lymphocytes 250
9-1 B-cell activation requires cross-linking of
surface immunoglobulin 250
Detailed Contents xiii
9-2 B-cell activation requires signals from the
B-cell co-receptor 250
9-3 The antibody response to certain antigens
does not require T-cell help 251
9-4 Activation of naive B cells by most antigens
requires help from CD4 T cells 254
9-5 The primary focus of clonal expansion in
the medullary cords produces plasma cells
secreting IgM 256
9-6 Follicular dendritic cells provide long-lasting
depositories of B-cell antigens 256
9-7 Activated B cells undergo somatic hypermutation
and isotype switching in the specialized
microenvironment of the B-cell zone 257
9-8 Selection of centrocytes by antigen in the
germinal center drives affinity maturation
of the B-cell response 259
9-9 The cytokines made by helper T cells
determine how B cells switch their
immunoglobulin isotype 261
9-10 Cytokines made by helper T cells determine
the differentiation of antigen-activated
B cells into plasma cells or memory cells 262
Summary 262
Antibody effector functions 263
9-11 IgM, IgG, and monomeric IgA protect the
internal tissues of the body 264
9-12 Dimeric IgA protects the mucosal surfaces
of the body 266
9-13 IgE provides a mechanism for the rapid
ejection of pathogens from the body 267
9-14 Mothers provide protective antibodies to
their young, both before and after birth 268
9-15 High-affinity neutralizing antibodies prevent
viruses and bacteria from infecting cells 268
9-16 High-affinity IgG and IgA antibodies are
used to neutralize microbial toxins and
animal venoms 270
9-17 Binding of IgM to antigen on a pathogen s
surface activates complement by the
classical pathway 272
9-18 Two forms of C4 tend to be fixed at different
sites on pathogen surfaces 273
9-19 Complement activation by IgG requires the
participation of two or more IgG molecules 274
9-20 Erythrocytes facilitate the removal of
immune complexes from the circulation 275
9-21 The four subclasses of IgG have different
and complementary functions 275
9-22 Fc receptors enable hematopoietic cells to bind
and be activated by IgG bound to pathogens 278
9-23 A variety of low-affinity Fc receptors are
specific for IgG 280
9-24 IgE binds to high-affinity Fc receptors on mast
cells, basophils, and activated eosinophils 282
9-25 The Fc receptor for monomeric IgA belongs
to a different family from the Fc receptors
for IgG and IgE 284
Summary 285
Summary to Chapter 9 285
Questions 286
Detailed Contents
Chapter 10
The Body s Defenses Against Infection 289
Preventing infection at mucosal surfaces 290
10-1 The communication functions of mucosal
surfaces render them vulnerable to infection 290
10-2 The gastrointestinal tract is invested with
distinctive secondary lymphoid tissues 291
10-3 M cells and dendritic cells facilitate transport
of microbes from the gut lumen to
gut-associated lymphoid tissues 293
10-4 Effector lymphocytes populate healthy
mucosal tissue in the absence of infection 294
10-5 B cells and T cells commit to mucosal
lymphoid tissues after they encounter their
specific antigen 296
10-6 Effector lymphocytes activated in any one
mucosal tissue recirculate through all
mucosal tissues 298
10-7 Dimeric IgA binds pathogens at various sites
in mucosal tissues 298
10-8 Two subclasses of IgA have complementary
properties for controlling microbial
populations 299
10-9 Humans with selective deficiency of IgA do
not succumb to infection 300
10-10 Intestinal epithelial cells contribute to innate
defense of the gut 301
10-11 Intestinal helminth infections provoke strong
Tn2-mediated immune responses 301
Summary 302
Immunological memory and the secondary
immune response 303
10-12 The antibodies formed during a primary
immune response prevent reinfection for
several months after disease 304
10-13 Immunological memory is sustained by clones
of long-lived memory T cells and B cells 305
10-14 Vaccination against a pathogen can generate
immunological memory that persists for life 306
10-15 Pathogen-specific memory B cells are more
abundant and make better antibodies than
do naive B cells 307
10-16 Activation of a secondary response involves
cell-cell interactions like those activating the
primary response 308
10-17 Only memory B cells, and not naive B cells,
participate in the secondary immune
response 308
10-18 Immune-complex mediated inhibition of
naive B cells is used to prevent hemolytic
anemia of the newborn 309
10-19 In the response to influenza virus,
immunological memory is gradually eroded 310
10-20 Several cell-surface markers distinguish
memory T cells from naive T cells 311
10-21 Two types of memory T cell function in
different tissues 313
10-22 Maintenance of immunological memory
is not dependent on antigen 313
Summary 314
Bridging innate and adaptive immunity 315
10-23 x T cells contribute to the innate immune
response 315
10-24 Individual NK cells express many different
combinations of receptors belonging to one
of two receptor families 317
10-25 NK cells use receptors for MHC class I
molecules to identify infected cells 318
10-26 NK cells have inhibitory receptors with different
specificities for MHC class 1 molecules 319
10-27 Inhibitory receptors for self MHC class I
make NK cells tolerant to self and responsive
to loss of MHC class I 321
10-28 T cells recognizing lipid antigens protect
against mycobacterial infection 322
10-29 NK T cells are cells of innate immunity that
express a:(J T-cell receptors 323
Summary 323
Summary to Chapter 10 324
Questions 326
Chapter 11
Failures of the Body s Defenses 329
Evasion and subversion of the immune
system by pathogens 329
11-1 Genetic variation within some species of
pathogens prevents effective long-term
immunity 330
11-2 Mutation and recombination allow influenza
virus to escape from immunity 330
11-3 Trypanosomes use gene rearrangement to
change their surface antigens 332
11-4 Herpesviruses persist in human hosts by
hiding from the immune response 333
11-5 Certain pathogens sabotage or subvert
immune defense mechanisms 334
11-6 Bacterial superantigens stimulate a massive
but ineffective T-cell response 336
11-7 Immune responses can contribute to disease 337
Summary 337
Inherited immunodeficiency diseases 338
11-8 Rare primary immunodeficiency diseases reveal
how the human immune system works 338
11-9 Inherited immunodeficiency diseases are
caused by dominant, recessive, or X-linked
gene defects 339
11-10 Recessive and dominant mutations in the
interferon-y receptor cause diseases of
differing severity 340
11-11 Antibody deficiency leads to an inability to
clear extracellular bacteria 341
11-12 Diminished production of antibodies also
results from inherited defects in T-cell help 343
11-13 Defects in complement components impair
antibody responses and cause the
accumulation of immune complexes 343
11-14 Defects in phagocytes result in enhanced
susceptibility to bacterial infection 345
11-15 Defects in T-cell function result in severe
combined immune deficiencies 346
11-16 Some inherited immunodeficiencies lead to
specific disease susceptibilities 348
11-17 Transplantation of hematopoietic stem cells
is used to correct genetic defects of the
immune system 349
Summary 351
Acquired immune deficiency syndrome 351
11-18 HIV is a retrovirus that causes slowly
progressing disease 351
11-19 HIV infects CD4 T cells, macrophages, and
dendritic cells 352
11-20 Most people who become infected with HIV
progress in time to develop AIDS 353
11-21 Genetic deficiency of the CCR5 co-receptor
for HIV confers resistance to infection 356
11 -22 HLA and KIR polymorphisms influence the
progression to AIDS 356
11 -23 HIV escapes the immune response and
develops resistance to antiviral drugs by
rapid mutation 357
11-24 Clinical latency is a period of active infection
and renewal of CD4 T cells 358
11-25 HIV infection leads to immunodeficiency
and death from opportunistic infections 359
Summary 360
Summary to Chapter 11 361
Questions 361
Chapter 12
Over-reactions of the Immune System 365
12-1 Four types of hypersensitivity reaction are
caused by different effector mechanisms of
adaptive immunity 365
Type I hypersensitivity reactions 367
12-2 IgE binding to FceRl provides mast cells,
basophils, and activated eosinophils with
antigen receptors 367
12-3 Mast cells defend and maintain the tissues
where they live 368
12-4 Tissue mast cells orchestrate IgE-mediated
allergic reactions through the release of
inflammatory mediators 370
12-5 Eosinophils are specialized granulocytes
that release toxic mediators in IgE-mediated
responses 371
12-6 Basophils are rare granulocytes that initiate
TH2 responses and the production of IgE 373
12-7 Very few antigens that enter the human body
are allergens that stimulate an IgE response 374
12-8 Predisposition to allergic disease has a
genetic basis 376
12-9 IgE-mediated allergic reactions consist of
an immediate response followed by a
late-phase response 377
12-10 The effects of IgE-mediated allergic reactions
vary with the site of mast-cell activation 378
12-11 Systemic anaphylaxis is caused by allergens
in the blood 379
12-12 Rhinitis and asthma are caused by inhaled
allergens 380
Detailed Contents xv
12-13 Urticaria, angioedema, and eczema are
allergic reactions in the skin 381
12-14 Food allergies cause systemic effects as well
as gut reactions 382
12-15 People with parasite infections and high
levels of IgE rarely develop allergic disease 383
12-16 Allergic reactions are prevented and treated
by three complementary approaches 384
Summary 385
Type II, III, and IV hypersensitivity
reactions 386
12-17 Type II hypersensitivity reactions are caused
by antibodies specific for altered components
of human cells 386
12-18 To avoid type II hypersensitivity reactions in
blood transfusion, donors and recipients are
matched for ABO antigens 387
12-19 Type III hypersensitivity reactions are caused
by immune complexes formed from IgG and
soluble antigens 389
12-20 Systemic disease caused by immune
complexes can follow the administration
of large quantities of soluble antigens 390
12-21 Inhaled antigens can cause type III
hypersensitivity reactions 392
12-22 Type IV hypersensitivity reactions are mediated
by antigen-specific effector T cells 392
12-23 Celiac disease is caused by hypersensitivity
to common food proteins 395
12-24 Severe hypersensitivity reactions to certain
drugs are strongly correlated with HLA
class I allotypes 397
Summary 398
Summary to Chapter 12 398
Questions 399
Chapter 13
Disruption of Healthy Tissue by the Immune
Response 403
Autoimmune diseases 403
13-1 In healthy individuals the immune system
is tolerant of self antigens 404
13-2 Autoimmune diseases are caused by the
loss of tolerance to self antigens 404
13-3 The effector mechanisms of autoimmunity
resemble those causing hypersensitivity
reactions 405
13-4 Endocrine glands contain specialized cells
that are targets for organ-specific
autoimmunity 407
13-5 Autoimmune diseases of the thyroid can cause
either underproduction or overproduction
of thyroid hormones 408
13-6 Ectopic lymphoid tissue can form at sites
inflamed by autoimmune disease 409
13-7 The cause of an autoimmune disease can be
revealed by the transfer of the disease by
immune effectors 410
13-8 Type 1 diabetes is caused by the selective
destruction of insulin-producing cells in
the pancreas 411
n Detailed Contents
13-9 Autoantibodies against common
components of human cells can cause
systemic autoimmune disease 412
13-10 Most rheumatological diseases are caused
by autoimmunity 413
13-11 Rheumatoid arthritis can be treated with
monoclonal antibodies that target either
TNF-oc or B cells 413
13-12 Multiple sclerosis and myasthenia gravis are
autoimmune diseases of the nervous system 414
Summary 416
Genetic and environmental factors
predispose to autoimmune disease 417
13-13 All autoimmune diseases involve breaking
T-cell tolerance 417
13-14 Incomplete deletion of self-reactive T cells in
the thymus causes autoimmune disease 417
13-15 Insufficient control of T-cell co-stimulation
favors autoimmunity 418
13-16 Regulatory T cells protect cells and tissues
from autoimmunity 419
13-17 HLA is the dominant genetic factor affecting
susceptibility to autoimmune disease 420
13-18 Different combinations of HLA class II
allotypes confer susceptibility and resistance
to diabetes 422
13-19 Autoimmunity is initiated by disease-
associated HLA allotypes presenting antigens
to autoimmune T cells 424
13-20 Noninfectious environmental factors influence
the course of autoimmune diseases 425
13-21 Genetic and environmental effects combine
to cause one form of rheumatoid arthritis 426
13-22 Infections are environmental factors that can
trigger autoimmune disease 427
13-23 Autoimmune T cells can be activated in a
pathogen-specific or nonspecific manner
by infection 428
13-24 In the course of autoimmune disease the
specificity of the autoimmune response
broadens 430
13-25 Senescence of the T-cell population can
contribute to autoimmunity 432
13-26 Does the current increase in hypersensitivity
and autoimmune disease have a common
cause? 432
Summary 433
Summary to Chapter 13 433
Questions 434
Chapter 14
Vaccination to Prevent Infectious Disease 437
14-1 Viral vaccines are made from whole viruses
or viral components 437
14-2 Bacterial vaccines are made from whole
bacteria, their secreted toxins, or capsular
polysaccharides 439
14-3 Adjuvants nonspecifically enhance the
immune response 441
14-4 Vaccination can inadvertently cause disease 443
14-5 The need for a vaccine and the demands
placed on it change with the prevalence of
the disease 444
14-6 Vaccines have yet to be found for many
chronic pathogens 446
14-7 Genome sequences of human pathogens
open up new avenues of vaccine design 447
14-8 A useful vaccine against HIV has yet to be
found 449
14-9 An effective and acceptable rotavirus vaccine
has been developed 450
14-10 Vaccine development faces greater public
scrutiny than drug development 450
Summary to Chapter 14 451
Questions 452
Chapter 15
Transplantation of Tissues and Organs 455
15-1 Transplant rejection and graft-versus-host
reaction are immune responses caused by
genetic differences between transplant
donors and recipients 455
15-2 Blood transfusion is the most widespread
kind of transplantation in clinical medicine 456
Transplantation of solid organs 458
15-3 Antibodies against ABO or HLA antigens
cause hyperacute rejection of transplanted
organs 458
15-4 Anti-HLA antibodies can arise from
pregnancy, blood transfusion, or previous
transplants 459
15-5 Organ transplantation involves procedures
that inflame the donated organ and the
transplant recipient 460
15-6 Acute rejection is caused by effector T cells
responding to HLA differences between
donor and recipient 460
15-7 HLA differences between transplant donor
and recipient activate numerous alloreactive
T cells 462
15-8 Negative selection in the thymus limits the
number of expressed MHC isoforms 462
15-9 Chronic rejection of organ transplants is
due to the indirect pathway of
allorecognition 462
15-10 Matching donor and recipient for HLA class I
and class II allotypes improves the outcome
of organ transplantation 466
15-11 Allogeneic transplantation is made possible
by the use of three types of
immunosuppressive drug 466
15-12 Corticosteroids change patterns of gene
expression 467
15-13 Cytotoxic drugs kill proliferating cells 469
15-14 Cyclosporin A, tacrolimus, and rapamycin
selectively inhibit T-cell activation 470
15-15 Antibodies specific forT cells are used to
prevent and control acute rejection 472
15-16 Patients needing a transplant outnumber
the available organs 473
15-17 The need for HLA matching and
immunosuppressive therapy varies with
the organ transplanted 474
Summary 475
Transplantation of hematopoietic stem cells 476
15-18 Bone marrow transplantation is a treatment
for genetic diseases of blood cells 476
15-19 Allogeneic bone marrow transplantation is
the preferred treatment for many cancers 477
15-20 The alloreactions in bone marrow
transplantation attack the patient, not the
transplant 477
15-21 Matching donor and recipient for HLA class I
and II is particularly important in bone
marrow transplantation 479
15-22 HLA-identical bone marrow transplants
cause GVHD through recognition of minor
histocompatibility antigens 480
15-23 Some GVHD helps engraftment and prevents
relapse of malignant disease 481
15-24 NK cells also mediate GVL effects 482
15-25 Hematopoietic cell transplantation can induce
tolerance to solid organ transplants 483
Summary 484
Summary to Chapter 15 484
Questions 485
Detailed Contents xvii
Chapter 16
Cancer and Its Interactions with the Immune
System 489
16-1 Cancer results from mutations that cause
uncontrolled cell growth 490
16-2 A cancer arises from a single cell that has
accumulated multiple mutations 491
16-3 Exposure to chemicals, radiation, and viruses
can facilitate the progression to cancer 492
16-4 Certain common features distinguish cancer
cells from normal cells 494
16-5 Immune responses to cancer have similarities
with those to virus-infected cells 494
16-6 Differences in MHC class I allow tumor
cells to be attacked and eliminated by
cytotoxic T cells 495
16-7 Mutations in cellular genes acquired during
oncogenesis provide tumor-specific
antigens 496
16-8 Cancer/testis antigens are a prominent type
of tumor-associated antigen 498
16-9 Successful tumors evade and manipulate
the immune response 498
16-10 By preventing infection, vaccination protects
against cancers caused by viruses 500
16-11 Vaccination with tumor antigens can cause
cancer to regress 500
16-12 Increasing co-stimulation can boost theT-cell
response to tumor cells 501
16-13 Heat-shock proteins can provide natural
adjuvants of tumor immunity 501
16-14 Monoclonal antibodies against cell-surface
tumor antigens can be used for diagnosis
and immunotherapy 502
Summary to Chapter 16 504
Questions 505
|
| any_adam_object | 1 |
| author | Parham, Peter 1950- |
| author_GND | (DE-588)136599443 |
| author_facet | Parham, Peter 1950- |
| author_role | aut |
| author_sort | Parham, Peter 1950- |
| author_variant | p p pp |
| building | Verbundindex |
| bvnumber | BV035368052 |
| callnumber-first | Q - Science |
| callnumber-label | QR181 |
| callnumber-raw | QR181 |
| callnumber-search | QR181 |
| callnumber-sort | QR 3181 |
| callnumber-subject | QR - Microbiology |
| classification_rvk | WF 9800 |
| ctrlnum | (OCoLC)240989634 (DE-599)BVBBV035368052 |
| dewey-full | 616.07/9 |
| dewey-hundreds | 600 - Technology (Applied sciences) |
| dewey-ones | 616 - Diseases |
| dewey-raw | 616.07/9 |
| dewey-search | 616.07/9 |
| dewey-sort | 3616.07 19 |
| dewey-tens | 610 - Medicine and health |
| discipline | Biologie Medizin |
| edition | 3. ed. |
| format | Book |
| fullrecord | <?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>02337nam a2200613zc 4500</leader><controlfield tag="001">BV035368052</controlfield><controlfield tag="003">DE-604</controlfield><controlfield tag="005">20090512 </controlfield><controlfield tag="007">t</controlfield><controlfield tag="008">090313s2009 xxuad|| |||| 00||| eng d</controlfield><datafield tag="010" ind1=" " ind2=" "><subfield code="a">2008034011</subfield></datafield><datafield tag="020" ind1=" " ind2=" "><subfield code="a">9780815341468</subfield><subfield code="9">978-0-8153-4146-8</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(OCoLC)240989634</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-599)BVBBV035368052</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-604</subfield><subfield code="b">ger</subfield><subfield code="e">aacr</subfield></datafield><datafield tag="041" ind1="0" ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="044" ind1=" " ind2=" "><subfield code="a">xxu</subfield><subfield code="c">US</subfield></datafield><datafield tag="049" ind1=" " ind2=" "><subfield code="a">DE-29</subfield></datafield><datafield tag="050" ind1=" " ind2="0"><subfield code="a">QR181</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">616.07/9</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">WF 9800</subfield><subfield code="0">(DE-625)148471:</subfield><subfield code="2">rvk</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Parham, Peter</subfield><subfield code="d">1950-</subfield><subfield code="e">Verfasser</subfield><subfield code="0">(DE-588)136599443</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">The immune system</subfield><subfield code="c">Peter Parham</subfield></datafield><datafield tag="250" ind1=" " ind2=" "><subfield code="a">3. ed.</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="a">London [u.a.]</subfield><subfield code="b">Garland Science</subfield><subfield code="c">c2009</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">XVII, 506, [83] S.</subfield><subfield code="b">zahlr. Ill., graph. Darst.</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="b">n</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="b">nc</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="650" ind1=" " ind2="2"><subfield code="a">Immunité</subfield></datafield><datafield tag="650" ind1=" " ind2="2"><subfield code="a">Système immunitaire</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immune system</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immunopathology</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immune System</subfield></datafield><datafield tag="650" ind1=" " ind2="4"><subfield code="a">Immunity</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Immunsystem</subfield><subfield code="0">(DE-588)4026643-6</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Immunbiologie</subfield><subfield code="0">(DE-588)4072743-9</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Immunreaktion</subfield><subfield code="0">(DE-588)4133841-8</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Krebs</subfield><subfield code="g">Medizin</subfield><subfield code="0">(DE-588)4073781-0</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Autoaggressionskrankheit</subfield><subfield code="0">(DE-588)4003935-3</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="650" ind1="0" ind2="7"><subfield code="a">Immunpathologie</subfield><subfield code="0">(DE-588)4014133-0</subfield><subfield code="2">gnd</subfield><subfield code="9">rswk-swf</subfield></datafield><datafield tag="689" ind1="0" ind2="0"><subfield code="a">Immunsystem</subfield><subfield code="0">(DE-588)4026643-6</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="0" ind2="1"><subfield code="a">Immunreaktion</subfield><subfield code="0">(DE-588)4133841-8</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="0" ind2="2"><subfield code="a">Krebs</subfield><subfield code="g">Medizin</subfield><subfield code="0">(DE-588)4073781-0</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="0" ind2="3"><subfield code="a">Autoaggressionskrankheit</subfield><subfield code="0">(DE-588)4003935-3</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="0" ind2=" "><subfield code="8">1\p</subfield><subfield code="5">DE-604</subfield></datafield><datafield tag="689" ind1="1" ind2="0"><subfield code="a">Immunsystem</subfield><subfield code="0">(DE-588)4026643-6</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="1" ind2="1"><subfield code="a">Immunpathologie</subfield><subfield code="0">(DE-588)4014133-0</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="1" ind2="2"><subfield code="a">Immunbiologie</subfield><subfield code="0">(DE-588)4072743-9</subfield><subfield code="D">s</subfield></datafield><datafield tag="689" ind1="1" ind2=" "><subfield code="8">2\p</subfield><subfield code="5">DE-604</subfield></datafield><datafield tag="856" ind1="4" ind2="2"><subfield code="m">HBZ Datenaustausch</subfield><subfield code="q">application/pdf</subfield><subfield code="u">http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=017171988&sequence=000004&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA</subfield><subfield code="3">Inhaltsverzeichnis</subfield></datafield><datafield tag="999" ind1=" " ind2=" "><subfield code="a">oai:aleph.bib-bvb.de:BVB01-017171988</subfield></datafield><datafield tag="883" ind1="1" ind2=" "><subfield code="8">1\p</subfield><subfield code="a">cgwrk</subfield><subfield code="d">20201028</subfield><subfield code="q">DE-101</subfield><subfield code="u">https://d-nb.info/provenance/plan#cgwrk</subfield></datafield><datafield tag="883" ind1="1" ind2=" "><subfield code="8">2\p</subfield><subfield code="a">cgwrk</subfield><subfield code="d">20201028</subfield><subfield code="q">DE-101</subfield><subfield code="u">https://d-nb.info/provenance/plan#cgwrk</subfield></datafield></record></collection> |
| id | DE-604.BV035368052 |
| illustrated | Illustrated |
| indexdate | 2024-07-09T21:32:16Z |
| institution | BVB |
| isbn | 9780815341468 |
| language | English |
| lccn | 2008034011 |
| oai_aleph_id | oai:aleph.bib-bvb.de:BVB01-017171988 |
| oclc_num | 240989634 |
| open_access_boolean | |
| owner | DE-29 |
| owner_facet | DE-29 |
| physical | XVII, 506, [83] S. zahlr. Ill., graph. Darst. |
| publishDate | 2009 |
| publishDateSearch | 2009 |
| publishDateSort | 2009 |
| publisher | Garland Science |
| record_format | marc |
| spelling | Parham, Peter 1950- Verfasser (DE-588)136599443 aut The immune system Peter Parham 3. ed. London [u.a.] Garland Science c2009 XVII, 506, [83] S. zahlr. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Immunité Système immunitaire Immune system Immunopathology Immune System Immunity Immunsystem (DE-588)4026643-6 gnd rswk-swf Immunbiologie (DE-588)4072743-9 gnd rswk-swf Immunreaktion (DE-588)4133841-8 gnd rswk-swf Krebs Medizin (DE-588)4073781-0 gnd rswk-swf Autoaggressionskrankheit (DE-588)4003935-3 gnd rswk-swf Immunpathologie (DE-588)4014133-0 gnd rswk-swf Immunsystem (DE-588)4026643-6 s Immunreaktion (DE-588)4133841-8 s Krebs Medizin (DE-588)4073781-0 s Autoaggressionskrankheit (DE-588)4003935-3 s 1\p DE-604 Immunpathologie (DE-588)4014133-0 s Immunbiologie (DE-588)4072743-9 s 2\p DE-604 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=017171988&sequence=000004&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis 1\p cgwrk 20201028 DE-101 https://d-nb.info/provenance/plan#cgwrk 2\p cgwrk 20201028 DE-101 https://d-nb.info/provenance/plan#cgwrk |
| spellingShingle | Parham, Peter 1950- The immune system Immunité Système immunitaire Immune system Immunopathology Immune System Immunity Immunsystem (DE-588)4026643-6 gnd Immunbiologie (DE-588)4072743-9 gnd Immunreaktion (DE-588)4133841-8 gnd Krebs Medizin (DE-588)4073781-0 gnd Autoaggressionskrankheit (DE-588)4003935-3 gnd Immunpathologie (DE-588)4014133-0 gnd |
| subject_GND | (DE-588)4026643-6 (DE-588)4072743-9 (DE-588)4133841-8 (DE-588)4073781-0 (DE-588)4003935-3 (DE-588)4014133-0 |
| title | The immune system |
| title_auth | The immune system |
| title_exact_search | The immune system |
| title_full | The immune system Peter Parham |
| title_fullStr | The immune system Peter Parham |
| title_full_unstemmed | The immune system Peter Parham |
| title_short | The immune system |
| title_sort | the immune system |
| topic | Immunité Système immunitaire Immune system Immunopathology Immune System Immunity Immunsystem (DE-588)4026643-6 gnd Immunbiologie (DE-588)4072743-9 gnd Immunreaktion (DE-588)4133841-8 gnd Krebs Medizin (DE-588)4073781-0 gnd Autoaggressionskrankheit (DE-588)4003935-3 gnd Immunpathologie (DE-588)4014133-0 gnd |
| topic_facet | Immunité Système immunitaire Immune system Immunopathology Immune System Immunity Immunsystem Immunbiologie Immunreaktion Krebs Medizin Autoaggressionskrankheit Immunpathologie |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=017171988&sequence=000004&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
| work_keys_str_mv | AT parhampeter theimmunesystem |