Immunology for the rheumatologist:
Saved in:
| Format: | Book |
|---|---|
| Language: | English |
| Published: |
Philadelphia [u.a.]
Saunders
2004
|
| Series: | Rheumatic disease clinics of North America
30,1 |
| Subjects: | |
| Online Access: | Inhaltsverzeichnis |
| Physical Description: | X, 235 S. Ill., graph. Darst. |
Staff View
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| 245 | 1 | 0 | |a Immunology for the rheumatologist |c guest ed. Bruce N. Cronstein |
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IMMUNOLOGY FOR THE RHT UMATOLOGET
CONTENTS
Preface ix
Bruce N. Cronstein
Complement and Immunity 1
Hector Molina
Our body is in constant interaction with the environment. Some
of the interactions involve the recognition and disposal of foreign
substances that may harm the delicate balance between health
and disease. The foreign elements, or antigens, include infectious
organisms and lifeless macromolecules. The ability of the body to
recognize what is dangerous and what is inconsequential, and to
refrain from damaging what is perceived as self, are the main
functions of the immune system. One important component of
the innate immune response is the complement system. This arti¬
cle describes the different mechanisms of how complement is
activated and the consequence of this activation, followed by a
characterization of the complement's role in inflammation and
autoimmunity, and the therapeutic considerations emanating from
these studies.
Phagocytes: Mechanisms of Inflammation and Tissue Destruction 19
Hongtao Liu and Richard M. Pope
Macrophages and neutrophils are the professional phagocytes of
the innate immune system. Once in the inflammatory joint or the
vasculitic lesion, macrophages and neutrophils contribute to the
pathology observed. This article examines the mechanisms by
which phagocytes contribute to the pathogenesis of these diseases.
Cytokines in the Rheumatic Diseases 41
William P. Arend and Cem Gabay
Extensive data has accumulated over the last 10 to 15 years to
implicate various cytokines in pathways of pathophysiology in
VOLUME 30 • NUMBER 1 • FEBRUARY 2004 v
rheumatic diseases. Abnormalities in cytokine production are not the
cause of these diseases, but reflect continual production by immune
and inflammatory cells. Cytokines are heterogeneous and function in
an overlapping and redundant network. An important principle to
emerge is that the net biologic response in a diseased organ or tissue
reflects a balance between the local levels of proinflammatory and
anti inflammatory cytokines and factors. Thus, a chronic disease may
result from the excess production of proinflammatory cytokines or
the inadequate production of anti inflammatory cytokines. This arti¬
cle summarizes the role of cytokines in rheumatic diseases by focus¬
ing on each disease and the involved pathways of pathophysiology.
Novel Endogenous Small Molecules as the Checkpoint
Controllers in Inflammation and Resolution: Entree for
Resoleomics 69
Charles N. Serhan and Nan Chiang
It is well appreciated that endogenous chemical mediators play key
roles in controlling inflammation. Recently, it has become increas¬
ingly apparent that novel mediators play a role in resolution.
Among them, lipoxins (LXs) and aspirin triggered LXs evoke
actions of interest in a range of physiologic and pathophysiologic
processes, and, thus, represent the first class of lipid/chemical medi¬
ators that are "switched on" in the resolution phase of an inflamma¬
tory reaction. Recently, novel arrays of endogenous local autocoids
were identified from dietary polyunsaturated fatty acids that dis¬
play potent anti inflammatory and proresolving actions and thus
are termed "resolvins." These previously unappreciated "check¬
point controllers" provide new opportunities to design "resolution
targeted" therapies with high degree of precision in controlling
inflammatory responses. This article provides an overview and
updates of the actions of LXs, their association with human diseases
as well as on the actions of recently uncovered resolvins.
Vascular Endothelium and Immune Responses: Implications
for Inflammation and Angiogenesis 97
Zoltan Szekanecz and Alisa E. Koch
Endothelial cells (ECs) are involved in several mechanisms during
the immune response, particularly in inflammation. Leukocyte
EC adhesion is regulated by the interactions of receptor ligand
adhesion molecule pairs, as well as by soluble mediators, such as
proinflammatory cytokines. ECs are active participants in new
vessel formation termed "angiogenesis." There have been several
attempts to therapeutically interfere with the cellular and molecular
mechanisms described above. Specific targeting of pathologic
endothelial function may be useful for the future management of
various inflammatory diseases.
vi CONTENTS
Dendritic Cells: Friend or Foe in Autoimmunity? 115
Frances Santiago Schwarz
This article summarizes recent advances in dendritic cell (DC) biol¬
ogy as related to normal and abnormal physiology. The large
amount of information acquired from human and animal models
substantiates that the DC lineage system represents a double edged
sword in the immune system and a critical link between innate and
acquired immunity. Presumably, in normal physiology, tolerizing
DCs guard against autoimmunity and control established immune
reactions, whereas immunogenic DCs provide active host defenses.
In autoimmune diseases, there is strong evidence to support the
idea that tolerance is overridden by the development of immuno¬
genic DCs that favor cross priming and stimulation of autoreactive
lymphocyte responses.
Biology of T Lymphocytes 135
Abbe N. Vallejo, Eduardo Davila, Cornelia M. Weyand,
and Jorg J. Goronzy
The biology of T cells is reviewed. T cell ontogeny, differentiation of
effector functions, tolerance, memory, senescence, and the cellular
and molecular mechanisms that regulate T cell mediated immune
responses are discussed with consideration to their applicability
to human disease pathogenesis. As appropriate, new paradigms or
paradigm shifts are presented.
B Cell Biology 159
Elena Weinstein, Elena Peeva, Chaim Putterman,
and Betty Diamond
B lymphocyte functions can be divided broadly into antigen pre¬
sentation and production of antibodies. Defects in either of these
functions may lead to immunodeficiency or autoimmunity. For the
rheumatologist, it is important to understand B cell development,
maturation, and activation to fully comprehend how alterations in
these processes shape the B cell repertoire and can lead eventually
to autoimmunity and organ pathology. The goal of this article is to
demonstrate how small changes in the selection of the B cell reper¬
toire, can, over time, and with the necessary environmental influ¬
ences, lead to rheumatic disease.
Costimulatory Molecules and T Cell B Cell Interactions 175
Mary K. Crow
This article focuses on activating and inhibiting costimulatory sig¬
nals that are delivered to the T cell from antigen presenting cells,
mediating and modulating T cell clonal expansion and development
of effector functions, as well as costimulatory signals that are deliv¬
ered by activated T cells to interacting target cells. The coordinated
CONTENTS vii
expression and interaction of these molecules regulates responses
to foreign antigens and avoidance of response to self antigens.
Knowledge of the structure and function of these costimulatory
molecules can be used to manipulate immune function and inhibit
autoimmunity and inflammation in the setting of disease.
Apoptosis and Immune Responses to Self 193
Jeannine S. Navratil, Janice M. Sabatine, and Joseph M. Ahearn
Most autoantibodies that are produced in patients who have sys¬
temic autoimmune diseases target proteins that are normally found
inside the cell, and many within the nucleus. Clues to how the
immune system becomes primed to recognize these intracellular
antigens and whether these autoantibodies contribute to the patho
genesis of autoimmune diseases are being uncovered by studying
apoptosis. The intracellular autoantigen targets of many systemic
autoimmune diseases become altered during apoptosis in ways
that may change how they are perceived by the immune system.
Under normal circumstances, apoptotic cells are cleared rapidly by
macrophages and dendritic cells, with the result that the apoptosis
altered self antigens are ignored by the immune system or toler¬
ance to those antigens is maintained actively. Defects in the process
whereby apoptotic cells are recognized and cleared may underlie
the development of systemic autoimmunity.
The Genetics of Autoimmune Mediated Rheumatic Diseases:
Clinical and Biologic Implications 213
Robert Winchester
This article emphasizes the interpretation of the meaning and signifi¬
cance of the genetic aspects of susceptibility to certain autoimmune
mediated rheumatic diseases. The familial aggregation and identical
twin concordance that provides the basis of considering these as
genetic diseases are reviewed. Major histocompatibility complex
(MHC) genes are taken as the primary examples of candidate genes
that regulate the immune response; the potential function of these
genes in predisposing to autoimmune diseases is analyzed. Auto¬
immune diseases are discussed as the consequence of the role of
MHC molecules encoded by different alleles that exhibit distinct
peptide binding properties and select a self reactive T cell repertoire.
The low penetrance rates of autoimmune mediated rheumatic dis¬
ease is used as an argument that stochastic events in the generation
and postthymic maturation of the somatically expressed T cell reper¬
toire account for the characteristically delayed onset of these dis¬
eases. The importance of self reactivity in the physiologic immune
response is used as an argument that the events that are responsible
for the development of an autoimmune disease are an untoward
exaggeration of normal immune responsiveness, but not a qualita¬
tively distinct biologic event.
Index 229
viii CONTENTS |
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| spelling | Immunology for the rheumatologist guest ed. Bruce N. Cronstein Philadelphia [u.a.] Saunders 2004 X, 235 S. Ill., graph. Darst. txt rdacontent n rdamedia nc rdacarrier Rheumatic disease clinics of North America 30,1 Immunology Rheumatism Immunological aspects Rheumatismus (DE-588)4049836-0 gnd rswk-swf Immunologie (DE-588)4026637-0 gnd rswk-swf (DE-588)4143413-4 Aufsatzsammlung gnd-content Rheumatismus (DE-588)4049836-0 s Immunologie (DE-588)4026637-0 s DE-604 Cronstein, Bruce N. Sonstige oth Rheumatic disease clinics of North America 30,1 (DE-604)BV000625464 30,1 HBZ Datenaustausch application/pdf http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&local_base=BVB01&doc_number=012040774&sequence=000002&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA Inhaltsverzeichnis |
| spellingShingle | Immunology for the rheumatologist Rheumatic disease clinics of North America Immunology Rheumatism Immunological aspects Rheumatismus (DE-588)4049836-0 gnd Immunologie (DE-588)4026637-0 gnd |
| subject_GND | (DE-588)4049836-0 (DE-588)4026637-0 (DE-588)4143413-4 |
| title | Immunology for the rheumatologist |
| title_auth | Immunology for the rheumatologist |
| title_exact_search | Immunology for the rheumatologist |
| title_full | Immunology for the rheumatologist guest ed. Bruce N. Cronstein |
| title_fullStr | Immunology for the rheumatologist guest ed. Bruce N. Cronstein |
| title_full_unstemmed | Immunology for the rheumatologist guest ed. Bruce N. Cronstein |
| title_short | Immunology for the rheumatologist |
| title_sort | immunology for the rheumatologist |
| topic | Immunology Rheumatism Immunological aspects Rheumatismus (DE-588)4049836-0 gnd Immunologie (DE-588)4026637-0 gnd |
| topic_facet | Immunology Rheumatism Immunological aspects Rheumatismus Immunologie Aufsatzsammlung |
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