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- Volume 15, 1997
Annual Review of Immunology - Volume 15, 1997
Volume 15, 1997
- Review Articles
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THE IMMUNE SYSTEM AS A SUPERSYSTEM
Vol. 15 (1997), pp. 1–13More LessI coined a term “supersystem” to designate highly integrated life systems such as the immune system, nervous system, and embryogenesis. While the mechanistic system is defined as a set of diverse elements so connected and related as to form an organic whole for a particular purpose, the “supersystem” engenders its own elements from a single progenitor. The diverse elements thus generated form relationships by mutual adaptation and coadaptation, and thus they create a dynamic self-regulating system through self-organization. It is a closed self-satisfied system, yet open to the environment, receiving outside signals to transduce them into internal messages for self-regulation and expansion. Unlike a mechanistic system, the “supersystem” has no defined purpose and determines its own fate by referring to its self-established behavioral pattern.
Both the immune and nervous systems develop and function as a typical “supersystem.” The prototype of the supersystem can be seen in embryogenesis and evolution. The concept of the supersystem can also be applied to the development of language, or a city, or other cultural phenomena that human beings have created as a result of their vital activities.
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HUMAN T CELL LEUKEMIA VIRUS TYPE I (HTLV-I) AND HUMAN DISEASES
Vol. 15 (1997), pp. 15–37More Less▪ AbstractHTLV-I infection is causally associated with a variety of human diseases including leukemia/lymphoma, myelopathy, uveitis, and arthropathy. Tax protein of HTLV-I, which is considered oncogenic, binds to transcription factors or other cytoplasmic cellular molecules involved in the fundamental cell function and thereby induces cellular changes. The interaction between HTLV-I–infected cells with dysregulated function and different kinds of cells in the host, such as lymphocytes and vascular endothelial cells through viral peptides, antigen receptors, cell adhesion molecules, and cytokines, appears to be one of the basic mechanisms underlying the development of HTLV-I–associated diseases. This interaction may play a major role in determining tumorigenicity and in forming clinical features of the diseases. The in vivo cell proliferation model of HTLV-I–infected cells using severe combined immunodeficient (SCID) mice can differentiate tumorigenicity from cell immortalization in vitro. The OX40 and its ligand gp34, which are induced by HTLV-I infection and directly mediate the adhesion between HTLV-I–infected T cells and vascular endothelial cells, may be critically involved in the localization and proliferation of HTLV-I–infected cells in vivo.
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THE MALE-SPECIFIC HISTOCOMPATIBILITY ANTIGEN, H-Y:A History of Transplantation, Immune Response Genes, Sex Determination and Expression Cloning
Vol. 15 (1997), pp. 39–61More Less▪ AbstractH-Y was originally discovered as a transplantation antigen. In vivo primary skin graft responses to H-Y are controlled by immune response (Ir) genes mapping to the MHC. In vitro T cell responses to H-Y are controlled by MHC class I and II Ir genes, which-respectively, restrict CD8 and CD4 T cells: These can be isolated as T cell clones in vitro. T cell receptor (TCR) transgenic mice have been made from the rearranged TCR genes of several of these, of which that specific for H-Y/Db is the best studied. Non-MHC Ir genes also contribute to the control of in vitro CTL responses to H-Y. The Hya/HYA gene(s) encoding H-Y antigen have been mapped using translocations, mutations, and deletions to Yq in humans and to the short arm of the Y chromosome in mice, where they lie in the deletion defined by the Sxrb mutation between Zfy-1 and Zfy-2. Hya/HYA has been separated from the testis-determining gene, Sry/SRY, in both humans and mice and in humans the azoospermia factor AZF has been separated from HYA. In mice transfection of cosmids and cDNAs mapping to the Sxrb deletion has identified two genes encoding H-Y peptide epitopes. Two such epitopes, H-Y/Kk and H-Y/Dk, are encoded within different exons of Smcy and a third, H-Y/Db, by a novel gene, Uty. Peptide elution approaches have isolated a human H-Y epitope, H-Y/HLA-B7, and identified it as a product of SMCY. Each of the Hya genes in mice is ubiquitously expressed but of unknown function. Their X chromosome homologues do not undergo X inactivation.
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LYME DISEASE:A Review of Aspects of Its Immunology and Immunopathogenesis
Vol. 15 (1997), pp. 63–92More Less▪ AbstractLyme disease, caused by Borrelia burgdorferi, causes a multisystem inflammatory ailment, although the precise means of tissue damage are not well understood. It is clear that the organism is present at the site of inflammation in many organs and that many of the features of the illness are relieved by antibiotic therapy. A complex interaction between spirochete and immune systems of a number of mammalian hosts, in human disease and animal models, has been described. It is clear that T cells and macrophages are intimately associated with the pathogenesis of arthritis and that immune mechanisms are involved in other aspects of disease. Inflammation directed at persistence of Borrelial antigens is a plausible explanation for persisting arthritis. Autoimmunity based on molecular mimicry may play a role in the pathogenesis of Lyme disease. Humoral immunity plays a protective role, prompting interest in vaccine development. Significant variation in certain of the outer surface proteins suggests that multiple proteins, peptides, or chimeric vaccines may be needed to provide a sufficiently broad humoral protective response.
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NATURALLY OCCURRING PRIMARY DEFICIENCIES OF THE IMMUNE SYSTEM
Vol. 15 (1997), pp. 93–124More Less▪ AbstractNaturally occurring genetic disorders of the immune system provide many models for the study of its development and function. In a way, their analysis complements the information provided by the generation of genetic defects in mice created using homologous recombination techniques. In this review, the recent findings made in three areas are focused upon deficiencies in T cell differentiation and in T lymphocyte activation, and on the control process of peripheral immune response.
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DIFFERENTIAL SIGNALING BY LYMPHOCYTE ANTIGEN RECEPTORS
Vol. 15 (1997), pp. 125–154More Less▪ AbstractStudies performed during the past several years make plain that ligand occupancy of antigen receptors need not necessarily provoke identical responses in all instances. For example, ligation of antigen receptors may stimulate a proliferative response, induce a state of unresponsiveness to subsequent stimulation (anergy), or induce apoptosis. How does a single type of transmembrane receptor induce these very heterogeneous cellular responses? In the following pages, we outline evidence supporting the view that the nature of the ligand/receptor interaction directs the physical recruitment of signaling pathways differentially inside the lymphocyte and hence defines the nature of the subsequent immune response. We begin by providing a functional categorization of antigen receptor components, considering the ways in which these components interact with the known set of signal transduction pathways, and then review the evidence suggesting that differential signaling through the TCR is achieved by qualitative differences in the effector pathways recruited by TCR, perhaps reflecting the time required to bring complicated signal transduction elements into proximity within the cell. The time-constant of the interaction between antigen and receptor in this way determines, at least in part, the nature of the resulting response. Finally, although our review focuses substantially on T cell receptor signaling, we have included a less detailed description of B cell receptor signaling as well, simply to emphasize the parallels that exist in these two closely related systems.
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THE ROLE OF THE IKAROS GENE IN LYMPHOCYTE DEVELOPMENT AND HOMEOSTASIS
Vol. 15 (1997), pp. 155–176More Less▪ AbstractThe Ikaros gene, which encodes a family of hemopoietic-specific zinc finger proteins, is described as a central regulator of lymphocyte differentiation. During fetal development, it is required at the earliest stage of T cell and B cell specification. In the adult, however, lymphoid lineages rely on Ikaros at distinct phases of their development. Its activity is essential for the generation of B cell but not of T cell precursors, although the differentiation of the latter is not normal. A significant increase in CD4 thymocytes and their immediate precursors is detected, and because these cells lack markers that correlate with positive selection, a deregulation in their maturation process is suggested. Furthermore, Ikaros-null thymocytes hyperproliferate in response to T cell receptor (TCR) signaling; within days after their appearance in the thymus, clonally expanding populations are detected. Deregulated TCR-mediated responses and the fast kinetics of tumor development in these mutant thymocytes implicate Ikaros as a central tumor suppressor gene for the T cell lineage. In addition, lack of natural killer cells and selective defects in γδ T cells and dendritic antigen-presenting cells point to Ikaros as an essential factor for the establishment of early branchpoints of the T cell pathway. The dominant interference activity of Ikaros isoforms unable to bind DNA and their effects in lymphocyte development suggest that Ikaros works in concert with other factors. The role of Aiolos, a lymphoid-restricted and structurally related gene, in lymphoid differentiation is discussed. A model is proposed that defines Ikaros as the backbone of a complex regulatory protein network that controls cell fate decisions and regulates homeostasis in the hemo-lymphoid system. Changes in this regulatory network may reflect differentiation and proliferation adjustments made in hemo-lymphoid progenitors and precursors as they give rise to the cells of our immune system.
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THE GENETIC DEFECT IN ATAXIA-TELANGIECTASIA
Vol. 15 (1997), pp. 177–202More Less▪ AbstractThe autosomal recessive human disorder ataxia-telangiectasia (A-T) was first described as a separate disease entity 40 years ago. It is a multisystem disease characterized by progressive cerebellar ataxia, oculocutaneous telangiectasia, radiosensitivity, predisposition to lymphoid malignancies and immunodeficiency, with defects in both cellular and humoral immunity. The pleiotropic nature of the clinical and cellular phenotype suggests that the gene product involved is important in maintaining stability of the genome but also plays a more general role in signal transduction. The chromosomal instability and radiosensitivity so characteristic of this disease appear to be related to defective activation of cell cycle checkpoints. Greater insight into the nature of the defect in A-T has been provided by the recent identification, by positional cloning, of the responsible gene, ATM. The ATM gene is related to a family of genes involved in cellular responses to DNA damage and/or cell cycle control. These genes encode large proteins containing a phosphatidylinositol 3-kinase domain, some of which have protein kinase activity. The mutations causing A-T completely inactivate or eliminate the ATM protein. This protein has been detected and localized to different subcellular compartments.
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Fc RECEPTOR BIOLOGY
Vol. 15 (1997), pp. 203–234More Less▪ AbstractThis review deals with membrane Fc receptors (FcR) of the immunoglobulin superfamily. It is focused on the mechanisms by which FcR trigger and regulate biological responses of cells on which they are expressed. FcR deliver signals when they are aggregated at the cell surface. The aggregation of FcR having immunoreceptor tyrosine-based activation motifs (ITAMs) activates sequentially src family tyrosine kinases and syk family tyrosine kinases that connect transduced signals to common activation pathways shared with other receptors. FcR with ITAMs elicit cell activation, endocytosis, and phagocytosis. The nature of responses depends primarily on the cell type. The aggregation of FcR without ITAM does not trigger cell activation. Most of these FcR internalize their ligands, which can be endocytosed, phagocytosed, or transcytosed. The fate of internalized receptor-ligand complexes depends on defined sequences in the intracytoplasmic domain of the receptors. The coaggregation of different FcR results in positive or negative cooperation. Some FcR without ITAM use FcR with ITAM as signal transduction subunits. The coaggregation of antigen receptors or of FcR having ITAMs with FcR having immunoreceptor tyrosine-based inhibition motifs (ITIMs) negatively regulates cell activation. FcR therefore appear as the subunits of multichain receptors whose constitution is not predetermined and which deliver adaptative messages as a function of the environment.
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NEUTRALIZING ANTIVIRAL B CELL RESPONSES
Vol. 15 (1997), pp. 235–270More Less▪ AbstractNeutralizing antiviral B cell responses differ in various aspects from the many usually measured B cell responses specific for protein in adjuvants. In particular, such neutralizing antiviral B cell responses are more rapidly induced, reach higher titers, are longer lived, and are efficiently generated without adjuvants. Evidence is summarized here that the repetitiveness of many viral antigens is a key factor responsible for the efficiency of these B cell responses, amplifying B cells early and rapidly for potent IgM responses and also for efficient switching to IgG. The data reviewed indicate that B cells discriminate antigen patterns via the degree of surface Ig-cross-linking and use antigen repetitiveness as a self/nonself discriminator.
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ESCAPE OF HUMAN IMMUNODEFICIENCY VIRUS FROM IMMUNE CONTROL
Vol. 15 (1997), pp. 271–296More Less▪ AbstractCytotoxic T lymphocytes (CTL) play a crucial role in the attempt to control infection with human immunodeficiency virus (HIV). Variation in epitopes recognized by CTL is common and frequently offers potential escape routes for mutant virus. Proof of escape, however, requires demonstration of increased frequency of virus particles or provirus that carry the escape sequence. There are now several recorded examples of virus variants that escape from CTL and are then selected. Most dramatic are those in which the CTL response has been dominated by CTL recognizing a single epitope that has suddenly changed, resulting in escape to fixation. This has been seen both early and late in the infection, leaving no doubt that escape occurs. Such escape is likely to be favored when the antiviral CTL response is oligoclonal and focused on a small number of immunodominant epitopes. The heterogeneous CTL response seen in many HIV-infected patients may result from successive waves of virus escape followed by new CTL responses specific for subdominant epitopes. Mutant virus can escape by several different routes, including failure of the mutated peptide to bind to the presenting HLA molecule and altered interactions with T cell receptors (TCR), including antagonism.
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INDUCTION OF TH1 AND TH2 CD4+ T CELL RESPONSES:The Alternative Approaches
Vol. 15 (1997), pp. 297–322More Less▪ AbstractT helper lymphocytes can be divided into two distinct subsets of effector cells based on their functional capabilities and the profile of cytokines they produce. The Th1 subset of CD4+ T cells secretes cytokines usually associated with inflammation, such as IFN-γ and TNF and induces cell-mediated immune responses. The Th2 subset produces cytokines such as IL-4 and IL-5 that help B cells to proliferate and differentiate and is associated with humoral-type immune responses. The selective differentiation of either subset is established during priming and can be significantly influenced by a variety of factors. One of these factors, the cytokine environment, has been put forward as the major variable influencing Th development and is already well reviewed by others. Instead, in the current review, we focus on some of the alternative approaches for skewing Th1/Th2 responses. Specifically, we discuss the effects on Th priming of (a) using altered peptide ligands as antigens, (b) varying the dose of antigen, and (c) altering costimulatory signals. The potential importance of each of these variables to influence immune responses to pathogens in vivo is discussed throughout.
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NITRIC OXIDE AND MACROPHAGE FUNCTION
Vol. 15 (1997), pp. 323–350More Less▪ AbstractAt the interface between the innate and adaptive immune systems lies the high-output isoform of nitric oxide synthase (NOS2 or iNOS). This remarkable molecular machine requires at least 17 binding reactions to assemble a functional dimer. Sustained catalysis results from the ability of NOS2 to attach calmodulin without dependence on elevated Ca2+. Expression of NOS2 in macrophages is controlled by cytokines and microbial products, primarily by transcriptional induction. NOS2 has been documented in macrophages from human, horse, cow, goat, sheep, rat, mouse, and chicken. Human NOS2 is most readily observed in monocytes or macrophages from patients with infectious or inflammatory diseases. Sustained production of NO endows macrophages with cytostatic or cytotoxic activity against viruses, bacteria, fungi, protozoa, helminths, and tumor cells. The antimicrobial and cytotoxic actions of NO are enhanced by other macrophage products such as acid, glutathione, cysteine, hydrogen peroxide, or superoxide. Although the high-output NO pathway probably evolved to protect the host from infection, suppressive effects on lymphocyte proliferation and damage to other normal host cells confer upon NOS2 the same protective/destructive duality inherent in every other major component of the immune response.
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REDOX REGULATION OF CELLULAR ACTIVATION
Vol. 15 (1997), pp. 351–369More Less▪ AbstractGrowing evidence has indicated that cellular reduction/oxidation (redox) status regulates various aspects of cellular function. Oxidative stress can elicit positive responses such as cellular proliferation or activation, as well as negative responses such as growth inhibition or cell death. Cellular redox status is maintained by intracellular redox-regulating molecules, including thioredoxin (TRX). TRX is a small multifunctional protein that has a redox-active disulfide/dithiol within the conserved active site sequence: Cys-Gly-Pro-Cys. Adult T cell leukemia–derived factor (ADF), which we originally defined as an IL-2 receptor α-chain/Tac inducer produced by human T cell lymphotrophic virus-I (HTLV-I)–transformed T cells, has been identified as human TRX. TRX/ADF is a stress-inducible protein secreted from cells. TRX/ADF has both intracellular and extracellular functions as one of the key regulators of signaling in the cellular responses against various stresses. Extracellularly, TRX/ADF shows a cytoprotective activity against oxidative stress–induced apoptosis and a growth-promoting effect as an autocrine growth factor. Intracellularly, TRX/ADF is involved in the regulation of protein-protein or protein–nucleic acid interactions through the reduction/oxidation of protein cysteine residues. For example, TRX/ADF translocates from the cytosol into the nucleus by a variety of cellular stresses, to regulate the expression of various genes through the redox factor-1 (Ref-1)/APEX. Further studies to clarify the regulatory roles of TRX/ADF and its target molecules may elucidate the intracellular signaling pathways in the responses against various stresses. The concept of “redox regulation” is emerging as an understanding of the novel mechanisms in the pathogenesis of several disorders, including viral infections, immunodeficiency, malignant transformation, and degenerative disease.
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LEUKOCYTE PROTEIN TYROSINE KINASES:Potential Targets for Drug Discovery
Vol. 15 (1997), pp. 371–404More Less▪ AbstractIntracellular signal transduction following the extracellular ligation of a wide variety of different types of surface molecules on leukocytes involves the activation of protein tyrosine kinases. The dependence of successful intracellular signaling on the functions of the nontransmembrane class of protein tyrosine kinases coupled with the cell type–specific expression patterns for several of these enzymes makes them appealing targets for therapeutic intervention. Development of drugs that can interfere with the catalytic functions of the nontransmembrane protein tyrosine kinases or that can disrupt critical interactions with regulatory molecules and/or substrates should find clinical applications in the treatment of allergic diseases, autoimmunity, transplantation rejection, and cancer.
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HUMAN CYTOTOXIC T LYMPHOCYTE RESPONSES TO EPSTEIN-BARR VIRUS INFECTION
Vol. 15 (1997), pp. 405–431More Less▪ AbstractEpstein-Barr virus (EBV) provides one of the most informative systems with which to study cytotoxic T lymphocyte (CTL) responses in humans. The virus establishes a highly immunogenic growth-transforming infection of B lymphocytes, associated with the coordinate expression of six virus-coded nuclear antigens (EBNAs 1, 2, 3A, 3B, 3C, -LP) and two latent membrane proteins (LMPs 1 and 2). This elicits both primary and memory CT8+ CTL responses that are markedly skewed toward HLA allele-specific epitopes drawn from the EBNA3A, 3B, 3C subset of latent proteins, with reactivities to other antigens being generally much less frequent. This heirarchy of immunodominance among the different latent proteins may at least partly reflect their differential accessibility to the HLA class I–processing pathway. Furthermore, CTLs to some of the immunodominant epitopes involve highly conserved T cell receptor (TCR) usage, a level of focusing which evidence suggests could have immunopathological consequences from cross-reactive recognition of other target structures. EBV is associated with a range of human tumors, and there is increasing interest in the possibility of targeting such malignancies using virus-specific CTLs. The dramatic reversal of EBV-driven lymphoproliferations in bone marrow transplant patients following CTL infusion demonstrates the potential of this approach, and here we discuss prospects for its extension to other EBV-positive tumors in which the immunodominant EBNA3A, 3B, 3C proteins are not expressed.
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STRUCTURE AND FUNCTION OF THE PRE-T CELL RECEPTOR
Vol. 15 (1997), pp. 433–452More Less▪ AbstractThe pre-T cell receptor (pre-TCR) that minimally consists of the TCRβ chain and the disulfide-linked pre-T cell receptor alpha (pTα) chain in association with signal-transducing CD3 molecules rescues from programmed cell death cells with productive TCRβ rearrangements. The pre-TCR induces expansion and differentiation of these cells such that they become TCRαβ bearing CD4+8+ thymocytes, which express only a single TCRβ chain and then either die of neglect or—upon TCR-ligand interaction—undergo either positive or negative selection. The newly discovered pTα gene encodes a transmembrane protein that belongs to the Ig superfamily and contains a cytoplasmic tail that, however, has no essential function in signal transduction, which is mediated by CD3 molecules and most likely p56lck. Experiments in pTα gene–deficient mice show that the pre-TCR has a crucial role in maturation as well as allelic exclusion of αβ T cells but is not required for the development of γδ-expressing cells. The function of the pre-TCR cannot be fully assumed by an αβ TCR that is expressed abnormally early in T cell development.
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INITIATION AND PROCESSING OF SIGNALS FROM THE B CELL ANTIGEN RECEPTOR
Michael Reth, and J. WienandsVol. 15 (1997), pp. 453–479More LessCurrent models of signal transduction from the antigen receptors on B and T cells still resemble equations with several unknown elements. Data from recent knock-out experiments in cell lines and mice contradict the assumption that Src-family kinase and tyrosine kinases of the Syk/Zap-70 family are the transducer elements that set signaling from these receptors in motion. Using a functional definition of signaling elements, we discuss the current knowledge of signaling events from the BCR and suggest the existence of an as-yet-unknown BCR transducer complex.
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CD22, A B LYMPHOCYTE–SPECIFIC ADHESION MOLECULE THAT REGULATES ANTIGEN RECEPTOR SIGNALING*1
Vol. 15 (1997), pp. 481–504More Less▪ AbstractThe development of B lymphocytes is a highly regulated process that depends in part on lineage-specific cell surface molecules. In addition, transmembrane signals generated through the B cell antigen receptor and other surface molecules regulate B cell responses to foreign antigens. Recent studies reveal CD22 to be a functionally significant receptor during these processes. CD22 is first expressed in the cytoplasm of pro-B and pre-B cells, and on the surface as B cells mature to become IgD+. CD22 is a member of the Ig superfamily that serves as an adhesion receptor for sialic acid-bearing ligands expressed on erythrocytes and all leukocyte classes. In addition to its potential role as a mediator of intercellular interactions, signal transduction through CD22 can activate B cells and modulate antigen receptor signaling in vitro. CD22 signaling is mediated via interactions with a number of kinases and phosphatases that bind the cytoplasmic domain through phosphorylated tyrosine residues located within consensus TAM and TIM motifs. The phenotype of CD22-deficient mice suggests that CD22 is primarily involved in the generation of mature B cells within the bone marrow, blood, and marginal zones of lymphoid tissues. Most notable in CD22-deficient mice is a significant diminution of surface Ig levels in these B cell subpopulations, which suggests that CD22 functions in vivo to adjust the signaling threshold of cell surface antigen receptors. A further understanding of CD22 function is required and may reveal roles for CD22 in disease susceptibility or the development of autoimmunity.
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CYTOKINE REGULATION OF HOST DEFENSE AGAINST PARASITIC GASTROINTESTINAL NEMATODES:Lessons from Studies with Rodent Models*1
Vol. 15 (1997), pp. 505–533More Less▪ AbstractStudies with rodents infected with Trichinella spiralis, Heligmosomoides polygyrus, Nippostrongylus brasiliensis, and Trichuris muris have provided considerable information about immune mechanisms that protect against parasitic gastrointestinal nematodes. Four generalizations can be made: 1. CD4+ T cells are critical for host protection; 2. IL-12 and IFN-γ inhibit protective immunity; 3. IL-4 can: (a) be required for host protection, (b) limit severity of infection, or (c) induce redundant protective mechanisms; and 4. Some cytokines that are stereotypically produced in response to gastrointestinal nematode infections fail to enhance host protection against some of the parasites that elicit their production. Host protection is redundant at two levels: 1. IL-4 has multiple effects on the immune system and on gut physiology (discussed in this review), more than one of which may protect against a particular parasite; and 2. IL-4 is often only one of multiple stimuli that can induce protection. Hosts may have evolved the ability to recognize features that characterize parasitic gastrointestinal nematodes as a class as triggers for a stereotypic cytokine response, but not the ability to distinguish features of individual parasites as stimuli for more specific protective cytokine responses. As a result, hosts deploy a set of defense mechanisms against these parasites that together control infection by most members of that class, even though a specific defense mechanism may not be required to defend against a particular parasite and may even damage a host infected with that parasite.
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Previous Volumes
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Volume 42 (2024)
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Volume 41 (2023)
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Volume 40 (2022)
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Volume 39 (2021)
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Volume 38 (2020)
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Volume 37 (2019)
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Volume 36 (2018)
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Volume 35 (2017)
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Volume 34 (2016)
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Volume 33 (2015)
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Volume 32 (2014)
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Volume 31 (2013)
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Volume 30 (2012)
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Volume 29 (2011)
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Volume 28 (2010)
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Volume 27 (2009)
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Volume 26 (2008)
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Volume 25 (2007)
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Volume 24 (2006)
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Volume 23 (2005)
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Volume 22 (2004)
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Volume 21 (2003)
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Volume 20 (2002)
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Volume 19 (2001)
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Volume 18 (2000)
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Volume 17 (1999)
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Volume 16 (1998)
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Volume 15 (1997)
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Volume 14 (1996)
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Volume 13 (1995)
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Volume 12 (1994)
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Volume 11 (1993)
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Volume 10 (1992)
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Volume 9 (1991)
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Volume 8 (1990)
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Volume 7 (1989)
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Volume 6 (1988)
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Volume 5 (1987)
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Volume 4 (1986)
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Volume 3 (1985)
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Volume 2 (1984)
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Volume 1 (1983)
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Volume 0 (1932)