Immunobiology: the immune system in health and disease
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| Format: | Book |
|---|---|
| Language: | English |
| Published: |
New York, NY
Garland Publ. [u.a.]
2001
|
| Edition: | 5. ed. |
| Subjects: | |
| Online Access: | Inhaltsverzeichnis |
| Physical Description: | XVIII, 732 S. Ill., graph. Darst. 1 CD-ROM (12 cm) |
| ISBN: | 081533642X 0443070989 0443070997 |
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| 245 | 1 | 0 | |a Immunobiology |b the immune system in health and disease |c Charles A. Janeway ... |
| 250 | |a 5. ed. | ||
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| adam_text | CONTENTS
PART I | AN INTRODUCTION TO IMMUNOBIOLOGY AND INNATE IMMUNITY
Chapter 1 Basic Concepts in Immunology 1
Chapter 2 Innate Immunity 35
PART II | THE RECOGNITION OF ANTIGEN
Chapter 3 Antigen Recognition by B cell and T cell Receptors 93
Chapter 4 The Generation of Lymphocyte Antigen Receptors 123
Chapter 5 Antigen Presentation to T Lymphocytes 155
PART HI | THE DEVELOPMENT OF MATURE LYMPHOCYTE RECEPTOR
REPERTOIRES
Chapter 6 Signaling Through Immune System Receptors 187
Chapter 7 The Development and Survival of Lymphocytes 221
Iffflllll THE ADAPTIVE IMMUNE RESPONSE
Chapter 8 T Cell Mediated Immunity 295
Chapter 9 The Humoral Immune Response 341
Chapter 10 Adaptive Immunity to Infection 381
[partY] the immune system in health and disease
Chapter 11 Failures of Host Defense Mechanisms 425
Chapter 12 Allergy and Hypersensitivity 471
Chapter 13 Autoimmunity and Transplantation 501
Chapter 14 Manipulation of the Immune Response 553
Afterword Evolution of the Immune System: Past, Present, and Future,
by Charles A. Janeway, Jr. 597
Appendix I Immunologists Toolbox 613
Appendix II CD Antigens 661
Appendix III Cytokines and their Receptors 677
Appendix IV Chemokines and their Receptors 680
Appendix V Immunological Constants 681
Biographies 682
Glossary 683
Index 708
List of Headings
I Parti I AN INTRODUCTION TO IMMUNO
1 BIOLOGY AND INNATE IMMUNITY
Chapter 1 Basic Concepts in Immunology
The components of the immune system.
1 1 The white blood cells of the immune system derive from
precursors in the bone marrow.
1 2 Lymphocytes mature in the bone marrow or the thymus.
1 3 The peripheral lymphoid organs are specialized to trap antigen,
to allow the initiation of adaptive immune responses, and to
provide signals that sustain recirculating lymphocytes.
1 4 Lymphocytes circulate between blood and lymph.
Summary.
Principles of innate and adaptive immunity.
1 5 Most infectious agents induce inflammatory responses by
activating innate immunity.
1 6 Activation of specialized antigen presenting cells is a necessary
first step for induction of adaptive immunity.
1 7 Lymphocytes activated by antigen give rise to clones of antigen
specific cells that mediate adaptive immunity.
1 8 Clonal selection of lymphocytes is the central principle of
adaptive immunity.
1 9 The structure of the antibody molecule illustrates the central
puzzle of adaptive immunity.
1 10 Each developing lymphocyte generates a unique antigen
receptor by rearranging its receptor genes.
1 11 Lymphocyte development and survival are determined by signals
received through their antigen receptors.
1 12 Lymphocytes proliferate in response to antigen in peripheral
lymphoid organs, generating effector cells and immunological
memory.
1 13 Interaction with other cells as well as with antigen is necessary
for lymphocyte activation.
Summary.
The recognition and effector mechanisms of adaptive
immunity.
1 14 Antibodies deal with extracellular forms of pathogens and their
toxic products.
1 15 T cells are needed to control intracellular pathogens and to
activate B cell responses to most antigens.
1 16 T cells are specialized to recognize foreign antigens as peptide
fragments bound to proteins of the major histocompatibility
complex.
1 17 Two major types of T cell recognize peptides bound to proteins
of two different classes of MHC molecule.
1 18 Defects in the immune system result in increased susceptibility
to infection.
1 19 Understanding adaptive immune responses is important for the
control of allergies, autoimmune disease, and organ graft
rejection.
1 20 Vaccination is the most effective means of controlling infectious
diseases.
Summary.
Summary to Chapter 1.
Chapter 2 Innate Immunity
The front line of host defense.
2 1 Infectious agents must overcome innate host defenses to
establish a focus of infection.
2 2 The epithelial surfaces of the body are the first defenses against
infection.
2 3 After entering tissues, many pathogens are recognized, ingested,
and killed by phagocytes.
2 4 Pathogen recognition and tissue damage initiate an inflammatory
response.
Summary.
The complement system and innate immunity.
2 5 Complement is a system of plasma proteins that interacts with
pathogens to mark them for destruction by phagocytes.
2 6 The classical pathway is initiated by activation of the C1
complex.
2 7 The mannan binding lectin pathway is homologous to the
classical pathway.
2 8 Complement activation is largely confined to the surface on
which it is initiated.
2 9 Hydrolysis of C3 causes initiation of the alternative pathway of
complement.
2 10 Surface bound C3 convertase deposits large numbers of C3b
fragments on pathogen surfaces and generates C5 convertase
activity.
2 11 Phagocyte ingestion of complement tagged pathogens is
mediated by receptors for the bound complement proteins.
2 12 Small fragments of some complement proteins can initiate a
local inflammatory response.
2 13 The terminal complement proteins polymerize to form pores in
membranes that can kill certain pathogens.
2 14 Complement control proteins regulate all three pathways of
complement activation and protect the host from its destructive
effects.
Summary.
Receptors of the innate immune system.
2 15 Receptors with specificity for pathogen surfaces recognize
patterns of repeating structural motifs.
2 16 Receptors on phagocytes can signal the presence of pathogens.
2 17 The effects of bacterial lipopolysaccharide on macrophages are
mediated by CD14 binding to Toll like receptor 4.
2 18 Activation of Toll like receptors triggers the production of pro
inflammatory cytokines and chemokines, and the expression of
co stimulatory molecules.
Summary.
Induced innate responses to infection.
2 19 Activated macrophages secrete a range of cytokines that have a
variety of local and distant effects.
2 20 Chemokines released by phagocytes recruit cells to sites of
infection.
2 21 Cell adhesion molecules control interactions between leukocytes
and endothelial cells during an inflammatory response.
2 22 Neutrophils make up the first wave of cells that cross the blood
vessel wall to enter inflammatory sites.
2 23 Tumor necrosis factor a is an important cytokine that triggers
local containment of infection, but induces shock when released
systemically.
2 24 Cytokines released by phagocytes activate the acute phase
response.
2 25 Interferons induced by viral infection make several contributions
to host defense.
2 26 Natural killer cells are activated by interferons and macrophage
derived cytokines to serve as an early defense against certain
intracellular infections.
2 27 NK cells possess receptors for self molecules that inhibit their
activation against uninfected host cells.
2 28 Several lymphocyte subpopulations and natural antibodies
behave like intermediates between adaptive and innate immunity.
Summary.
Summary to Chapter 2.
Part II | THE RECOGNITION OF ANTIGEN
Chapter 3 Antigen Recognition by B cell and T cell
Receptors
The structure of a typical antibody molecule.
3 1 IgG antibodies consist of four polypeptide chains.
3 2 Immunoglobulin heavy and light chains are composed of
constant and variable regions.
3 3 The antibody molecule can readily be cleaved into functionally
distinct fragments.
3 4 The immunoglobulin molecule is flexible, especially at the hinge
region.
3 5 The domains of an immunoglobulin molecule have similar
structures.
Summary.
The interaction of the antibody molecule with specific antigen.
3 6 Localized regions of hypervariable sequence form the antigen
binding site.
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.
3 8 Antibodies bind to conformational shapes on the surfaces of
antigens.
3 9 Antigen antibody interactions involve a variety of forces.
Summary.
L
Antigen recognition by T cells.
3 10 The antigen receptor on T cells is very similar to a Fab fragment
of immunoglobulin.
3 11 A T cell receptor recognizes antigen in the form of a complex of
a foreign peptide bound to an MHC molecule.
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.
3 13 The two classes of MHC molecule are expressed differentially on
cells.
3 14 The two classes of MHC molecule have distinct subunit
structures but similar three dimensional structures.
3 15 Peptides are stably bound to MHC molecules, and also serve to
stabilize the MHC molecule on the cell surface.
3 16 MHC class I molecules bind short peptides of 8 10 amino acids
by both ends.
3 17 The length of the peptides bound by MHC class II molecules is
not constrained.
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.
3 19 A distinct subset of T cells bears an alternative receptor made up
of y and 5 chains.
Summary.
Summary to Chapter 3.
Chapter 4 The Generation of Lymphocyte Antigen
Receptors
The generation of diversity in immunoglobulins.
4 1 Immunoglobulin genes are rearranged in antibody producing
cells.
4 2 The DNA sequence encoding a complete V region is generated
by the somatic recombination of separate gene segments.
4 3 There are multiple different V region gene segments.
4 4 Rearrangement of V, D, and J gene segments is guided by
flanking DNA sequences.
4 5 The reaction that recombines V, D, and J gene segments
involves both lymphocyte specific and ubiquitous DNA modifying
enzymes.
4 6 The diversity of the immunoglobulin repertoire is generated by
four main processes.
4 7 The multiple inherited gene segments are used in different
combinations.
4 8 Variable addition and subtraction of nucleotides at the junctions
between gene segments contributes to diversity in the third
hypervariable region.
4 9 Rearranged V genes are further diversified by somatic
hypermutation.
4 10 In some species most immunoglobulin gene diversification
occurs after gene rearrangement.
Summary.
T cell receptor gene rearrangement.
4 11 The T cell receptor loci comprise sets of gene segments and are
rearranged by the same enzymes as the immunoglobulin loci.
4 12 T cell receptors concentrate diversity in the third hypervariable
region.
4 13 y:5 T cell receptors are also generated by gene rearrangement.
4 14 Somatic hypermutation does not generate diversity in T cell
receptors.
Summary.
Structural variation in immunoglobulin constant regions.
4 15 The immunoglobulin heavy chain isotypes are distinguished by
the structure of their constant regions.
4 16 The same Vh exon can associate with different Ch genes in the
course of an immune response.
4 17 Transmembrane and secreted forms of immunoglobulin are
generated from alternative heavy chain transcripts.
4 18 Antibody C regions confer functional specialization.
4 19 IgM and IgA can form polymers.
4 20 Various differences between immunoglobulins can be detected
by antibodies.
Summary.
Summary to Chapter 4.
Chapter 5 Antigen Presentation to T Lymphocytes
The generation of T cell receptor ligands.
5 1 The MHC class I and class II molecules deliver peptides to the
cell surface from two distinct intracellular compartments.
5 2 Peptides that bind to MHC class I molecules are actively
transported from the cytosol to the endoplasmic reticulum.
5 3 Peptides for transport into the endoplasmic reticulum are
generated in the cytosol.
5 4 Newly synthesized MHC class I molecules are retained in the
endoplasmic reticulum until they bind peptide.
5 5 Peptides presented by MHC class II molecules are generated in
acidified endocytic vesicles.
5 6 The invariant chain directs newly synthesized MHC class II
molecules to acidified intracellular vesicles.
5 7 A specialized MHC class ll like molecule catalyzes loading of
MHC class II molecules with peptides.
5 8 Stable binding of peptides by MHC molecules provides effective
antigen presentation at the cell surface.
Summary.
The major histocompatibility complex and its functions.
5 9 Many proteins involved in antigen processing and presentation
are encoded by genes within the major histocompatibility
complex.
5 10 A variety of genes with specialized functions in immunity are also
encoded in the MHC.
5 11 Specialized MHC class I molecules act as ligands for activation
and inhibition of NK cells.
5 12 The protein products of MHC class I and class II genes are
highly polymorphic.
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.
5 14 Nonself MHC molecules are recognized by 1 10% of T cells.
5 15 Many T cells respond to superantigens.
5 16 MHC polymorphism extends the range of antigens to which the
immune system can respond.
5 17 Multiple genetic processes generate MHC polymorphism.
5 18 Some peptides and lipids generated in the endocytic pathway
can be bound by MHC class Mike molecules that are encoded
outside the MHC.
Summary.
Summary to Chapter 5.
Part III I THE DEVELOPMENT OF MATURE
L LYMPHOCYTE RECEPTOR
REPERTOIRES
Chapter 6 Signaling Through Immune System
Receptors
General principles of transmembrane signaling.
6 1 Binding of antigen leads to clustering of antigen receptors on
lymphocytes.
6 2 Clustering of antigen receptors leads to activation of intracellular
signal molecules.
6 3 Phosphorylation of receptor cytoplasmic tails by tyrosine kinases
concentrates intracellular signaling molecules around the
receptors.
6 4 Intracellular signaling components recruited to activated
receptors transmit the signal onward from the membrane and
amplify it.
6 5 Small G proteins activate a protein kinase cascade that transmits
the signal to the nucleus.
Summary.
Antigen receptor structure and signaling pathways.
6 6 The variable chains of lymphocyte antigen receptors are
associated with invariant accessory chains that carry out the
signaling function of the receptor.
6 7 The ITAMs associated with the B cell and T cell receptors are
phosphorylated by protein tyrosine kinases of the Src family.
6 8 Antigen receptor signaling is enhanced by co receptors that bind
the same ligand.
6 9 Fully phosphorylated ITAMs bind the protein tyrosine kinases Syk
and ZAP 70 and enable them to be activated.
6 10 Downstream events are mediated by proteins that associate with
the phosphorylated tyrosines and bind to and activate other
proteins.
6 11 Antigen recognition leads ultimately to the induction of new gene
synthesis by activating transcription factors.
6 12 Not all ligands for the T cell receptor produce a similar response.
6 13 Other receptors on leukocytes also use ITAMs to signal
activation.
6 14 Antigen receptor signaling can be inhibited by receptors
associated with ITIMs.
Summary.
Other signaling pathways that contribute to lymphocyte
behavior.
6 15 Microbes and their products release NFkB from its site in the
cytosol through an ancient pathway of host defense against
infection.
6 16 Bacterial peptides, mediators of inflammatory responses, and
chemokines signal through members of the seven
transmembrane domain, trimeric G protein coupled receptor
family.
6 17 Cytokines signal lymphocytes by binding to cytokine receptors
and triggering Janus kinases to phosphorylate and activate STAT
proteins.
6 18 Programmed cell death of activated lymphocytes is triggered
mainly through the receptor Fas.
6 19 Lymphocyte survival is maintained by a balance between death
promoting and death inhibiting members of the Bcl 2 family of
proteins.
6 20 Homeostasis of lymphocyte populations is maintained by signals
that lymphocytes are continually receiving through their antigen
receptors.
Summary.
Summary to Chapter 6.
Chapter 7 The Development and Survival of
Lymphocytes
Generation of lymphocytes in bone marrow and thymus.
7 1 Lymphocyte development occurs in specialized environments
and is regulated by the somatic rearrangement of the antigen
receptor genes.
7 2 B cells develop in the bone marrow with the help of stromal cells
and achieve maturity in peripheral lymphoid organs.
7 3 Stages in B cell development are distinguished by the expression
of immunoglobulin chains and particular cell surface proteins.
7 4 T cells also originate in the bone marrow, but all the important
events in their development occur in the thymus.
7 5 Most developing T cells die in the thymus.
7 6 Successive stages in the development of thymocytes are marked
by changes in cell surface molecules.
7 7 Thymocytes at different developmental stages are found in
distinct parts of the thymus.
Summary.
The rearrangement of antigen receptor gene segments
controls lymphocyte development.
7 8 B cells undergo a strictly programmed series of gene
rearrangements in the bone marrow.
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.
7 10 Rearrangement at the immunoglobulin light chain locus leads to
cell surface expression of the B cell receptor.
7 11 The expression of proteins regulating immunoglobulin gene
rearrangement and function is developmental^ programmed.
7 12 T cells in the thymus undergo a series of gene segment
rearrangements similar to those of B cells.
7 13 T cells with a:p or y5 receptors arise from a common
progenitor.
7 14 T cells expressing particular y and 8 chain V regions arise in an
ordered sequence early in life.
7 15 Rearrangement of the (3 chain locus and production of a p chain
trigger several events in developing thymocytes.
7 16 T cell cc chain genes undergo successive rearrangements until
positive selection or cell death intervenes.
Summary.
Interaction with self antigens selects some lymphocytes for
survival but eliminates others.
7 17 Immature B cells that bind self antigens undergo futher receptor
rearrangement, or die, or are inactivated.
7 18 Mature B cells can also be rendered self tolerant.
7 19 Only thymocytes whose receptors can interact with self MHC:self
peptide complexes can survive and mature.
7 20 Most thymocytes express receptors that cannot interact with self
MHC and these cells die in the thymus.
7 21 Positive selection acts on a repertoire of receptors with inherent
specificity for MHC molecules.
7 22 Positive selection coordinates the expression of CD4 or CD8 with
the specificity of the T cell receptor and the potential effector
functions of the cell.
7 23 Thymic cortical epithelial cells mediate positive selection of
developing thymocytes.
7 24 T cells that react strongly with ubiquitous self antigens are
deleted in the thymus.
7 25 Negative selection is driven most efficiently by bone marrow
derived antigen presenting cells.
7 26 Endogenous superantigens mediate negative selection of T cell
receptors derived from particular Vp gene segments.
7 27 The specificity and strength of signals for negative and positive
selection must differ.
7 28 The B 1 subset of B cells has a distinct developmental history
and expresses a distinctive repertoire of receptors.
Summary.
Survival and maturation of lymphocytes in peripheral
lymphoid tissues.
7 29 Newly formed lymphocytes home to particular locations in
peripheral lymphoid tissues.
7 30 The development and organization of peripheral lymphoid tissues
is controlled by cytokines and chemokines.
7 31 Only a small fraction of immature B cells mature and survive in
peripheral lymphoid tissues.
7 32 The life span of naive T cells in the periphery is determined by
ongoing contact with self peptide:seif MHC complexes similar to
those that initially selected them.
7 33 B cell tumors often occupy the same site as their normal
counterparts.
7 34 A range of tumors of immune system cells throws light on
different stages of T cell development.
7 35 Malignant lymphocyte tumors frequently carry chromosomal
translocations that join immunoglobulin loci to genes regulating
cell growth.
Summary.
Summary to Chapter 7.
J*ft# THE ADAPTIVE IMMUNE
** RESPONSE
Chapter 8 T Cell Mediated Immunity
The production of armed effector T cells.
8 1 T cell responses are initiated in peripheral lymphoid organs by
activated antigen presenting cells.
8 2 Naive T cells sample the MHC:peptide complexes on the surface
of antigen presenting cells as they migrate through peripheral
lymphoid tissue.
8 3 Lymphocyte migration, activation, and effector function depend
on cell cell interactions mediated by cell adhesion molecules.
8 4 The initial interaction of T cells with antigen presenting cells is
mediated by cell adhesion molecules.
8 5 Both specific ligand and co stimulatory signals provided by an
antigen presenting cell are required for the clonal expansion of
naive T cells.
8 6 Dendritic cells specialize in taking up antigen and activating
naive T cells.
8 7 Macrophages are scavenger cells that can be induced by
pathogens to present foreign antigens to naive T cells.
8 8 B cells are highly efficient at presenting antigens that bind to their
surface immunoglobulin.
8 9 Activated T cells synthesize the T cell growth factor interleukin 2
and its receptor.
8 10 The co stimulatory signal is necessary for the synthesis and
secretion of IL 2.
8 11 Antigen recognition in the absence of co stimulation leads to
T cell tolerance.
8 12 Proliferating T cells differentiate into armed effector T cells that
do not require co stimulation to act.
8 13 The differentiation of CD4 T cells into TH1 or TH2 cells
determines whether humoral or cell mediated immunity will
predominate.
8 14 Naive CD8 T cells can be activated in different ways to become
armed cytotoxic effector cells.
Summary.
General properties of armed effector T cells.
8 15 Effector T cell interactions with target cells are initiated by
antigen nonspecific cell adhesion molecules.
8 16 Binding of the T cell receptor complex directs the release of
effector molecules and focuses them on the target cell.
8 17 The effector functions of T cells are determined by the array of
effector molecules they produce.
8 18 Cytokines can act locally or at a distance.
8 19 Cytokines and their receptors fall into distinct families of
structurally related proteins.
8 20 The TNF family of cytokines are trimeric proteins that are often
associated with the cell surface.
Summary.
T cell mediated cytotoxicity.
8 21 Cytotoxic T cells can induce target cells to undergo programmed
cell death.
8 22 Cytotoxic effector proteins that trigger apoptosis are contained in
the granules of CD8 cytotoxic T cells.
8 23 Activated CD8 T cells and some CD4 effector T cells express
Fas ligand, which can also activate apoptosis.
8 24 Cytotoxic T cells are selective and serial killers of targets
expressing specific antigen.
8 25 Cytotoxic T cells also act by releasing cytokines.
Summary.
Macrophage activation by armed CD4 TH1 cells.
8 26 Armed Th1 cells have a central role in macrophage activation.
8 27 The production of cytokines and membrane associated
molecules by armed CD4 TH1 cells requires new RNA and
protein synthesis.
8 28 Activation of macrophages by armed TH1 cells promotes
microbial killing and must be tightly regulated to avoid tissue
damage.
8 29 Th1 cells coordinate the host response to intracellular
pathogens.
Summary.
Summary to Chapter 8.
Chapter 9 The Humoral Immune Response
B cell activation by armed helper T cells.
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.
9 2 Armed helper T cells activate B cells that recognize the same
antigen.
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.
9 4 Isotype switching requires expression of CD40L by the helper
T cell and is directed by cytokines.
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.
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.
9 7 Germinal center B cells undergo V region somatic hypermutation
and cells with mutations that improve affinity for antigen are
selected.
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.
9 9 Surviving germinal center B cells differentiate into either plasma
cells or memory cells.
9 10 B cell responses to bacterial antigens with intrinsic ability to
activate B cells do not require T cell help.
9 11 B cell responses to bacterial polysaccharides do not require
peptide specific T cell help.
Summary.
The distribution and functions of immunoglobulin isotypes.
9 12 Antibodies of different isotype operate in distinct places and have
distinct effector functions.
9 13 Transport proteins that bind to the Fc regions of antibodies carry
particular isotypes across epithelial barriers.
9 14 High affinity IgG and IgA antibodies can neutralize bacterial toxins.
9 15 High affinity IgG and IgA antibodies can inhibit the infectivity of
viruses.
9 16 Antibodies can block the adherence of bacteria to host cells.
9 17 Antibody:antigen complexes activate the classical pathway of
complement by binding to C1q.
9 18 Complement receptors are important in the removal of immune
complexes from the circulation.
Summary.
The destruction of antibody coated pathogens via Fc
receptors.
9 19 The Fc receptors of accessory cells are signaling receptors
specific for immunoglobulins of different isotypes.
9 20 Fc receptors on phagocytes are activated by antibodies bound to
the surface of pathogens and enable the phagocytes to ingest
and destroy pathogens.
9 21 Fc receptors activate natural killer cells to destroy antibody
coated targets.
9 22 Mast cells, basophils, and activated eosinophils bind IgE
antibody via the high affinity Fee receptor.
9 23 IgE mediated activation of accessory cells has an important role
in resistance to parasite infection.
Summary.
Summary to Chapter 9.
Chapter 10 Adaptive Immunity to Infection
Infectious agents and how they cause disease.
10 1 The course of an infection can be divided into several distinct
phases.
10 2 Infectious diseases are caused by diverse living agents that
replicate in their hosts.
Summary.
The course of the adaptive response to infection.
10 3 The nonspecific responses of innate immunity are necessary for
an adaptive immune response to be initiated.
10 4 An adaptive immune response is initiated when circulating T cells
encounter their corresponding antigen in draining lymphoid
tissues and become activated.
10 5 Cytokines made in the early phases of an infection influence the
functional differentiation of CD4 T cells.
10 6 Distinct subsets of T cells can regulate the growth and effector
functions of other T cell subsets.
10 7 The nature and amount of antigenic peptide can also affect the
differentiation of CD4 T cells.
10 8 Armed effector T cells are guided to sites of infection by
chemokines and newly expressed adhesion molecules.
10 9 Antibody responses develop in lymphoid tissues under the
direction of armed helper T cells.
10 10 Antibody responses are sustained in medullary cords and bone
marrow.
10 11 The effector mechanisms used to clear an infection depend on
the infectious agent.
10 12 Resolution of an infection is accompanied by the death of most
of the effector cells and the generation of memory cells.
Summary.
The mucosal immune system.
10 13 Mucosa associated lymphoid tissue is located in anatomically
defined microcompartments throughout the gut.
10 14 The mucosal immune system contains a distinctive repertoire of
lymphocytes.
10 15 Secretory IgA is the antibody isotype associated with the
mucosal immune system.
10 16 Most antigens presented to the mucosal immune system induce
tolerance.
10 17 The mucosal immune system can mount an immune response to
the normal bacterial flora of the gut.
10 18 Enteric pathogens cause a local inflammatory response and the
development of protective immunity.
10 19 Infection by Helicobacter pylori causes a chronic inflammatory
response, which may cause peptic ulcers, carcinoma of the
stomach, and unusual lymphoid tumors.
10 20 In the absence of inflammatory stimuli, the normal response of
the mucosal immune system to foreign antigens is tolerance.
Summary.
Immunological memory.
10 21 Immunological memory is long lived after infection or vaccination.
10 22 Both clonal expansion and clonal differentiation contribute to
immunological memory in B cells.
10 23 Repeated immunizations lead to increasing affinity of antibody
owing to somatic hypermutation and selection by antigen in
germinal centers.
L
10 24 Memory T cells are increased in frequency and have distinct
activation requirements and cell surface proteins that distinguish
them from armed effector T cells.
10 25 In immune individuals, secondary and subsequent responses are
mediated solely by memory lymphocytes and not by naive
lymphocytes.
Summary.
Summary to Chapter 10.
PartVl THE IMMUNE SYSTEM IN
HEALTH AND DISEASE
Chapter 11 Failures of Host Defense Mechanisms
Pathogens have evolved various means of evading or
subverting normal host defenses.
11 1 Antigenic variation allows pathogens to escape from immunity.
11 2 Some viruses persist in vivo by ceasing to replicate until
immunity wanes.
11 3 Some pathogens resist destruction by host defense mechanisms
or exploit them for their own purposes.
11 4 Immunosuppression or inappropriate immune responses can
contribute to persistent disease.
11 5 Immune responses can contribute directly to pathogenesis.
Summary.
Inherited immunodeficiency diseases.
11 6 A history of repeated infections suggests a diagnosis of
immunodeficiency.
11 7 Inherited immunodeficiency diseases are caused by recessive
gene defects.
11 8 The main effect of low levels of antibody is an inability to clear
extracellular bacteria.
11 9 T cell defects can result in low antibody levels.
11 10 Defects in complement components cause defective humoral
immune function.
11 11 Defects in phagocytic cells permit widespread bacterial
infections.
11 12 Defects in T cell function result in severe combined
immunodeficiencies.
11 13 Defective T cell signaling, cytokine production, or cytokine action
can cause immunodeficiency.
11 14 The normal pathways for host defense against intracellular
bacteria are illustrated by genetic deficiencies of IFN yand IL 12
and their receptors.
11 15 X linked lymphoproliferative syndrome is associated with fatal
infection by Epstein Barr virus and with the development of
lymphomas.
11 16 Bone marrow transplantation or gene therapy can be useful to
correct genetic defects.
Summary.
Acquired immune deficiency syndrome.
11 17 Most individuals infected with HIV progress over time to AIDS.
11 18 HIV is a retrovirus that infects CD4 T cells, dendritic cells, and
macrophages.
11 19 Genetic deficiency of the macrophage chemokine co receptor for
HIV confers resistance to HIV infection in vivo.
11 20 HIV RNA is transcribed by viral reverse transcriptase into DNA
that integrates into the host cell genome.
11 21 Transcription of the HIV provirus depends on host cell transcription
factors induced upon the activation of infected T cells.
11 22 Drugs that block HIV replication lead to a rapid decrease in titer
of infectious virus and an increase in CD4 T cells.
11 23 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.
11 24 Lymphoid tissue is the major reservoir of HIV infection.
11 25 An immune response controls but does not eliminate HIV.
11 26 HIV infection leads to low levels of CD4 T cells, increased
susceptibility to opportunistic infection, and eventually to death.
11 27 Vaccination against HIV is an attractive solution but poses many
difficulties.
11 28 Prevention and education are one way in which the spread of
HIV and AIDS can be controlled.
Summary.
Summary to Chapter 11.
Chapter 12 Allergy and Hypersensitivity
The production of IgE.
12 1 Allergens are often delivered transmucosally at low dose, a route
that favors IgE production.
12 2 Enzymes are frequent triggers of allergy.
12 3 Class switching to IgE in B lymphocytes is favored by specific
signals.
12 4 Genetic factors contribute to the development of IgE mediated
allergy, but environmental factors may also be important.
Summary.
Effector mechanisms in allergic reactions.
12 5 Most IgE is cell bound and engages effector mechanisms of the
immune system by different pathways from other antibody
isotypes.
12 6 Mast cells reside in tissues and orchestrate allergic reactions.
12 7 Eosinophils are normally under tight control to prevent
inappropriate toxic responses.
12 8 Eosinophils and basophils cause inflammation and tissue
damage in allergic reactions.
12 9 An allergic reaction is divided into an immediate response and a
late phase response.
12 10 The clinical effects of allergic reactions vary according to the site
of mast cell activation.
12 11 Allergen inhalation is associated with the development of rhinitis
and asthma.
12 12 Skin allergy is manifest as urticaria or chronic eczema.
12 13 Allergy to foods causes symptoms limited to the gut and systemic
reactions.
12 14 Allergy can be treated by inhibiting either IgE production or the
effector pathways activated by cross linking of cell surface IgE.
Summary.
Hypersensitivity diseases.
12 15 Innocuous antigens can cause type II hypersensitivity reactions
in susceptible individuals by binding to the surfaces of circulating
blood cells.
12 16 Systemic disease caused by immune complex formation can
follow the administration of large quantities of poorly catabolized
antigens.
12 17 Delayed type hypersensitivity reactions are mediated by Th1
cells and CD8 cytotoxic T cells.
Summary.
Summary to Chapter 12.
Chapter 13 Autoimmunity and Transplantation
Autoimmune responses are directed against self antigens.
13 1 Specific adaptive immune responses to self antigens can cause
autoimmune disease.
13 2 Autoimmune diseases can be classified into clusters that are
typically either organ specific or systemic.
13 3 Susceptibility to autoimmune disease is controlled by
environmental and genetic factors, especially MHC genes.
13 4 The genes that have been associated with the development of
systemic lupus erythematosus provide important clues to the
etiology of the disease.
13 5 Antibody and T cells can cause tissue damage in autoimmune
disease.
13 6 Autoantibodies against blood cells promote their destruction.
13 7 The fixation of sublytic doses of complement to cells in tissues
stimulates a powerful inflammatory response.
13 8 Autoantibodies against receptors cause disease by stimulating or
blocking receptor function.
13 9 Autoantibodies against extracellular antigens cause inflammatory
injury by mechanisms akin to type II and type III hypersensitivity
reactions.
13 10 Environmental cofactors can influence the expression of
autoimmune disease.
13 11 The pattern of inflammatory injury in autoimmunity can be
modified by anatomical constraints.
13 12 The mechanism of autoimmune tissue damage can often be
determined by adoptive transfer.
13 13 T cells specific for self antigens can cause direct tissue injury
and have a role in sustained autoantibody responses.
13 14 Autoantibodies can be used to identify the target of the
autoimmune process.
13 15 The target of T cell mediated autoimmunity is difficult to identify
owing to the nature of T cell ligands.
Summary.
Responses to alloantigens and transplant rejection.
13 16 Graft rejection is an immunological response mediated primarily
by T cells.
13 17 Matching donor and recipient at the MHC improves the outcome
of transplantation.
13 18 In MHC identical grafts, rejection is caused by peptides from
other alloantigens bound to graft MHC molecules.
13 19 There are two ways of presenting alloantigens on the transplant
to the recipient s T lymphocytes.
13 20 Antibodies reacting with endothelium cause hyperacute graft
rejection.
13 21 The converse of graft rejection is graft versus host disease.
13 22 Chronic organ rejection is caused by inflammatory vascular injury
to the graft.
13 23 A variety of organs are transplanted routinely in clinical medicine.
13 24 The fetus is an allograft that is tolerated repeatedly.
Summary.
Self tolerance and its loss.
13 25 Many autoantigens are not so abundantly expressed that they
induce clonal deletion or anergy but are not so rare as to escape
recognition entirely.
13 26 The induction of a tissue specific response requires the
presentation of antigen by antigen presenting cells with co
stimulatory activity.
13 27 In the absence of co stimulation, tolerance is induced.
13 28 Dominant immune suppression can be demonstrated in models
of tolerance and can affect the course of autoimmune disease.
13 29 Antigens in immunologically privileged sites do not induce
immune attack but can serve as targets.
13 30 B cells with receptors specific for peripheral autoantigens are
held in check by a variety of mechanisms.
13 31 Autoimmunity may sometimes be triggered by infection.
Summary.
Summary to Chapter 13.
Chapter 14 Manipulation of the Immune Response
Extrinsic regulation of unwanted immune responses.
14 1 Corticosteroids are powerful anti inflammatory drugs that alter
the transcription of many genes.
14 2 Cytotoxic drugs cause immunosuppression by killing dividing
cells and have serious side effects.
14 3 Cyclosporin A, FK506 (tacrolimus), and rapamycin (sirolimus) are
powerful immunosuppressive agents that interfere with T cell
signaling.
14 4 Immunosuppressive drugs are valuable probes of intracellular
signaling pathways in lymphocytes.
14 5 Antibodies against cell surface molecules have been used to
remove specific lymphocyte subsets or to inhibit cell function.
14 6 Antibodies can be engineered to reduce their immunogenicity
in humans.
14 7 Monoclonal antibodies can be used to inhibit allograft rejection.
14 8 Antibodies can be used to alleviate and suppress autoimmune
disease.
14 9 Modulation of the pattern of cytokine expression by
T lymphocytes can inhibit autoimmune disease.
14 10 Controlled administration of antigen can be used to manipulate
the nature of an antigen specific response.
Summary.
Using the immune response to attack tumors.
14 11 The development of transplantable tumors in mice led to the
discovery that mice could mount a protective immune response
against tumors.
14 12 T lymphocytes can recognize specific antigens on human tumors.
14 13 Tumors can escape rejection in many ways.
14 14 Monoclonal antibodies against tumor antigens, alone or linked to
toxins, can control tumor growth.
14 15 Enhancing the immunogenicity of tumors holds promise for
cancer therapy.
Summary.
Manipulating the immune response to fight infection.
14 16 There are several requirements for an effective vaccine.
L
14 17 The history of vaccination against Bordetella pertussis illustrates
the importance of developing an effective vaccine that is
perceived to be safe.
14 18 Conjugate vaccines have been developed as a result of
understanding how T and B cells collaborate in an immune
response.
14 19 The use of adjuvants is another important approach to enhancing
the immunogenicity of vaccines.
14 20 Live attenuated viral vaccines are usually more potent than
killed vaccines and can be made safer by using recombinant
DNA technology.
14 21 Live attenuated bacterial vaccines can be developed by selecting
nonpathogenic or disabled mutants.
14 22 Attenuated microorganisms can serve as vectors for vaccination
against many pathogens.
14 23 Synthetic peptides of protective antigens can elicit protective
immunity.
14 24 The route of vaccination is an important determinant of success.
14 25 Protective immunity can be induced by injecting DNA encoding
microbial antigens and human cytokines into muscle.
14 26 The effectiveness of a vaccine can be enhanced by targeting it to
sites of antigen presentation.
14 27 An important question is whether vaccination can be used
therapeutically to control existing chronic infections.
14 28 Modulation of the immune system might be used to inhibit
immunopathological responses to infectious agents.
Summary.
Summary to Chapter 14.
Afterword Evolution of the Immune System: Past,
Present, and Future, by
Charles A. Janeway, Jr.
Evolution of the innate immune system.
Innate immunity has its origins in early eukaryotes such as the
amoeba.
Sophisticated means of host defense were hard wired in the
genome by the time organisms diverged into plants and animals.
Fruit flies illustrate the virtues of a nonclonal system of host
defense.
Many genes that operate in fruit fly immunity also operate in
humans and plants and appear to be universal components of
host defense.
Summary.
Evolution of the adaptive immune response.
Adaptive immunity appears abruptly in the cartilaginous fish.
Gene rearrangement is used to control gene expression.
Animals generate antigen receptor diversity in many different
ways.
Summary.
The importance of immunological memory in fixing adaptive
immunity in the genome.
Immunological memory is the hallmark of adaptive immunity.
Immunological memory allows survival in a world filled with
pathogens.
Immunological memory for self proteins leads to autoimmune
disease.
Summary.
J
Future directions of research in immunobiology
Future studies should vastly expand our knowledge of innate
immunity.
Future studies should refine our knowledge of adaptive immunity.
Future studies of tumor immunity hold great promise for an
immunological cure for cancer.
Future vaccine development should greatly increase our ability to
prevent infectious disease.
Future studies of autoimmunity and graft rejection should allow
control of immune responses to one s own body or to a piece
borrowed from someone else.
Summary.
Summary of the Afterword.
Appendix I Immunologists Toolbox
Immunization.
A 1 Haptens.
A 2 Routes of immunization.
A 3 Effects of antigen dose.
A 4 Adjuvants.
The detection, measurement, and characterization of
antibodies and their use as research and diagnostic tools.
A 5 Affinity chromatography.
A 6 Radioimmunoassay (RIA), enzyme linked immunosorbent assay
(ELISA), and competitive inhibition assay.
A 7 Hemagglutination and blood typing.
A 8 Precipitin reaction.
A 9 Equilibrium dialysis: measurement of antibody affinity and
avidity.
A 10 Anti immunoglobulin antibodies.
A 11 Coombs tests and the detection of Rhesus incompatibility.
A 12 Monoclonal antibodies.
A 13 Phage display libraries for antibody V region production.
A 14 Immunofluorescence microscopy.
A 15 Immunoelectron microscopy.
A 16 Immunohistochemistry.
A 17 Immunoprecipitation and co immunoprecipitation.
A 18 Immunoblotting (Western blotting).
A 19 Use of antibodies in the isolation and identification of genes and
their products.
Isolation of lymphocytes.
A 20 Isolation of peripheral blood lymphocytes by Ficoll Hypaque™
gradient.
A 21 Isolation of lymphocytes from tissues other than blood.
A 22 Flow cytometry and FACS analysis.
A 23 Lymphocyte isolation using antibody coated magnetic beads.
A 24 Isolation of homogeneous T cell lines.
Characterization of lymphocyte specificity, frequency, and
function.
A 25 Limiting dilution culture.
A 26 ELISPOT assays.
A 27 Identification of functional subsets of T cells by staining for
cytokines.
A 28 Identification of T cell receptor specificity using MHC:peptide
tetramers.
A 29 Assessing the diversity of the T cell repertoire by spectratyping.
A 30 Biosensor assays for measuring the rates of association and
disassociation of antigen receptors for their ligands.
A 31 Stimulation of lymphocyte proliferation by treatment with
polyclonal mitogens or specific antigen.
A 32 Measurements of apoptosis by the TUNEL assay.
A 33 Assays for cytotoxic T cells.
A 34 Assays for CD4 T cells.
A 35 DNA microarrays.
Detection of immunity in vivo.
A 36 Assessment of protective immunity.
A 37 Transfer of protective immunity.
A 38 The tuberculin test.
A 39 Testing for allergic responses.
A 40 Assessment of immune responses and immunological
competence in humans.
A 41 The Arthus reaction.
Manipulation of the immune system.
A 42 Adoptive transfer of lymphocytes.
A 43 Hematopoietic stem cell transfers.
A 44 In vivo depletion of T cells.
A 45 In vivo depletion of B cells.
A 46 Transgenic mice.
A 47 Gene knockout by targeted disruption.
Appendix II CD Antigens
Appendix III Cytokines and their Receptors
Appendix IV Chemokines and their Receptors
Appendix V Immunological Constants
Biographies
Glossary
Index
|
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| dewey-sort | 3616.07 19 |
| dewey-tens | 610 - Medicine and health |
| discipline | Biologie Chemie Medizin |
| edition | 5. ed. |
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| id | DE-604.BV013492639 |
| illustrated | Illustrated |
| indexdate | 2024-07-09T18:46:46Z |
| institution | BVB |
| isbn | 081533642X 0443070989 0443070997 |
| language | English |
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| spelling | Immunobiology the immune system in health and disease Charles A. Janeway ... 5. ed. New York, NY Garland Publ. [u.a.] 2001 XVIII, 732 S. Ill., graph. Darst. 1 CD-ROM (12 cm) txt rdacontent n rdamedia nc rdacarrier Immunité Immunologie Immune System physiology Immune System physiopathology Immune system Immunity Immunity physiology Immunology Immunotherapy CD-ROM (DE-588)4139307-7 gnd rswk-swf Immunbiologie (DE-588)4072743-9 gnd rswk-swf Immunologie (DE-588)4026637-0 gnd rswk-swf (DE-588)4151278-9 Einführung gnd-content Immunbiologie (DE-588)4072743-9 s CD-ROM (DE-588)4139307-7 s DE-604 Immunologie (DE-588)4026637-0 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=009209027&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 Immunité Immunologie Immune System physiology Immune System physiopathology Immune system Immunity Immunity physiology Immunology Immunotherapy CD-ROM (DE-588)4139307-7 gnd Immunbiologie (DE-588)4072743-9 gnd Immunologie (DE-588)4026637-0 gnd |
| subject_GND | (DE-588)4139307-7 (DE-588)4072743-9 (DE-588)4026637-0 (DE-588)4151278-9 |
| title | Immunobiology the immune system in health and disease |
| 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 | Immunité Immunologie Immune System physiology Immune System physiopathology Immune system Immunity Immunity physiology Immunology Immunotherapy CD-ROM (DE-588)4139307-7 gnd Immunbiologie (DE-588)4072743-9 gnd Immunologie (DE-588)4026637-0 gnd |
| topic_facet | Immunité Immunologie Immune System physiology Immune System physiopathology Immune system Immunity Immunity physiology Immunology Immunotherapy CD-ROM Immunbiologie Einführung |
| url | http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=009209027&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA |
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