Critical Reviews in Immunology (CRIT REV IMMUNOL )

Publisher: Begell House


The great advances in immunology in recent years make this field one of the most rapidly growing in biological sciences. This remarkable growth is stimulated by the influx of investigators from other disciplines such as biochemistry, genetics, molecular biology, and by an increased number of investigators who came to immunology through the more traditional routes of microbiology and various medical disciplines. As a consequence, immunology has become a vast and rich field encompassing outlooks that range from the highly clinical to the highly molecular. Although such perspectives may appear diverse, they are, in fact, highly interdependent. Critical Reviews in Immunology presents a balanced overview of contemporary immunology and melds together molecular immunology and immunobiology.

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    Critical reviews in immunology, Chemical Rubber Company critical reviews in immunology, CRC critical reviews in immunology
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Begell House

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Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Immunologic memory is the adaptive immune system’s powerful ability to remember a previous antigen encounter and react with accelerated vigor upon antigen re-exposure. It provides durable protection against reinfection with pathogens and is the foundation for vaccine-induced immunity. Unlike the relatively restricted immunologic purview of memory B cells and CD8 T cells, the field of CD4 T-cell memory must account for multiple distinct lineages with diverse effector functions, the issue of lineage commitment and plasticity, and the variable distribution of memory cells within each lineage. Here, we discuss the evidence for lineage-specific CD4 T-cell memory and summarize the known factors contributing to memory-cell generation, plasticity, and long-term maintenance. PMID: 24940912
    Critical Reviews in Immunology 04/2014; 34(2):121-146.
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    ABSTRACT: Natural killer (NK) cells are important in protection against virus infections, and many viruses have evolved mechanisms to thwart NK cell activity. NK cells respond to inflammatory signals at an early stage of virus infection, resulting in proliferation, cytokine production, and cytolytic activity that can reduce virus loads. Moreover, the rapid kinetics of the NK cell response enables NK cells to influence other populations of innate immune cells, affect the inflammatory milieu, and guide adaptive immune responses to infection. Early NK cell interactions with other leukocytes can have long-lasting effects on the number and quality of memory T cells, as well as impact the exhaustion of T cells during chronic infections. The ability of NK cells to modulate T cell responses can be mediated through direct T-NK interactions, cytokine production, or indirectly through dendritic cells and other cell types. Herein, we summarize our current understanding of how NK cells interact with T cells, dendritic cells, B cells, and other cell types involved in adaptive immune responses to virus infection. We outline several mechanisms by which NK cells enhance or suppress adaptive immune response and long-lived immunological memory.
    Critical Reviews in Immunology 01/2014; 34(5):359-88.
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    ABSTRACT: Scavenger receptor A (SR-A), also known as the macrophage scavenger receptor and cluster of differentiation 204 (CD204), plays roles in lipid metabolism, atherogenesis, and a number of metabolic processes. However, recent evidence points to important roles for SR-A in inflammation, innate immunity, host defense, sepsis, and ischemic injury. Herein, we review the role of SR-A in inflammation, innate immunity, host defense, sepsis, cardiac and cerebral ischemic injury, Alzheimer's disease, virus recognition and uptake, bone metabolism, and pulmonary injury. Interestingly, SR-A is reported to be host protective in some disease states, but there is also compelling evidence that SR-A plays a role in the pathophysiology of other diseases. These observations of both harmful and beneficial effects of SR-A are discussed here in the framework of inflammation, innate immunity, and endoplasmic reticulum stress.
    Critical Reviews in Immunology 01/2014; 34(3):241-261.
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    ABSTRACT: Inflammasomes, multiprotein platforms of caspase-1 activation, are assembled in response to a number of exogenous and endogenous danger signals, leading to the production of pro-inflammatory cytokines and induction of inflammatory cell death through the activation of caspase-1. Inflammasomes have been implicated in a wide range of physiological and pathological processes, including host defense against microbial pathogens, maintenance of intestinal homeostasis, and even development of inflammatory disorders. Thus, inflammasomes can be both beneficial and detrimental, and understanding the mechanisms involved in inflammasome activation may provide a better approach to prevent the harmful effects of the inflammatory response. Although inflammasome complexes are formed via protein-protein interactions between their components, accumulating evidence suggests that inflammasome activation is positively and negatively regulated by ligand-binding receptors, accessory proteins, other caspases, cytokines, kinases/phosphatases, redox sensors, ion homeostasis, second messengers, organelles, cytoskeleton, and autophagy, among others. Moreover, inflammasome activation can result in the formation of another caspase-1-activating protein complex, the ASC speck/pyroptosome, which is also tightly controlled. In this review, we discuss how the assembly of inflammasomes and ASC speck is regulated by complex mechanisms. Recent findings on effector functions and biological roles of inflammasomes also are summarized.
    Critical Reviews in Immunology 01/2014; 34(1):41-80.
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    ABSTRACT: Adipose tissue historically was believed to be an inert tissue, functioning primarily in the storage of energy and thermal homeostasis. However, recent discoveries point toward a critical role for adipocytes in endocrine function as well as immune regulation. Excess body fat, accumulated through aging and/or a calorie-rich diet, is associated with many chronic metabolic and inflammatory diseases. Within the stromal vascular fraction of adipose tissue, macrophages and T cells accumulate with increasing tissue mass, secreting pro- or anti-inflammatory cytokines. In this review we discuss the current understanding of immune cell function in both diet-induced and age-related obesity. In both models of obesity, the classically activated, pro-inflammatory (M1) subtype takes precedence over the alternatively activated, anti-inflammatory (M2) macrophages, causing tissue necrosis and releasing pro-inflammatory cytokines like interleukin-6. Other distinct adipose tissue macrophage subtypes have been identified by surface marker expression and their functions characterized. Adipose tissue T cell recruitment to adipose tissue is also different between aging- and diet-induced obesity. Under both conditions, T cells exhibit restricted T-cell receptor diversity and produce higher levels of pro-inflammatory signals like interferon-γ and granzyme B relative to young or healthy mice. However, numbers of regulatory T cells are dramatically different between the 2 models of obesity. Taken together, these findings suggest models of age- and diet-induced obesity may be more distinct than previously thought, with many questions yet to be resolved in this multidimensional disease.
    Critical Reviews in Immunology 01/2014; 34(1):1-14.
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    ABSTRACT: Resolvin E1 (RvE1) is a recently discovered lipid-derived mediator that is endogenously synthesized from the polyunsaturated fatty acid eicosapentaenoic acid. RvE1 is locally generated in response to inflammation where it enhances the resolution phase of inflammation by diminishing neutrophil chemotaxis and by enhancing nonphlogistic macrophage-directed clearance of apoptotic neutrophils. RvE1 was also found to be effective in preventing and restoring bone loss in the inflammatory bone disease periodontitis. This review examines experimental evidence on RvEl's actions in bone. Current data indicate that in addition to anti-inflammatory actions, RvE1 also directly acts on bone cells and promotes bone preservation.
    Critical Reviews in Immunology 01/2014; 34(4):347-357.
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    ABSTRACT: It is now established that natural killer T (NKT) cells can influence adaptive immune responses by producing vast amounts of cytokines. Different subsets of NKT cells with distinctive functional characteristics regarding cytokine production have been described. This is the case for NKT1, NKT2, or NKT17 that resemble conventional CD4 Th1, Th2, and Th17 cells in the cytokines they produce. Unlike conventional CD4 T cells that mostly acquire functional specialization in the periphery, a number of NKT cells become specialized effectors during thymic development. This opinion article describes the evidence for an extrathymic commitment of specialized NKT-cell subsets that, together with thymic lineages, contributes to the overall functional diversity of NKT cells participating in immune responses in the periphery.
    Critical Reviews in Immunology 01/2014; 34(1):81-90.
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    ABSTRACT: Chemokines are chemotactic cytokines critical for homeostatic and inflammation-induced trafficking of leukocytes during immune responses, hematopoesis, wound healing, and tumorigenesis. Despite three decades of intensive study of the chemokine network, the molecular mechanisms regulating chemokine expression during tumor growth are not well understood. In this review, we focus on the role of chemokines in both tumor growth and anti-tumor immune responses and on molecular mechanisms employed by tumor cells to regulate chemokine expression in the tumor microenvironment. Multiple mechanisms used by tumors to regulate chemokine production, including those revealed by very recent studies (such as DNA methylation or post-translational nitrosylation of chemokines) are discussed. Concluding the review, we discuss how understanding of these regulatory mechanisms can be used in cancer therapy to suppress tumor growth and/or to promote immune-mediated eradication of tumors.
    Critical Reviews in Immunology 01/2014; 34(2):103-120.
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    ABSTRACT: Innate-like lymphocytes, which comprise an integral part of the immune system, possess unique developmental and functional capabilities that set them apart from conventional T and B lymphocytes. Strategically located to act as a first line of defense against pathogens, they behave as innate cells. To efficiently perform their innate functions, these populations are endowed with common phenotypic characteristics that include the expression of semi-invariant TCR or BCR and activation/memory cell markers. Moreover, they have the capacity to rapidly respond to pathogenic threats and the ability to ignite adaptive immune response in synchrony with myeloid cells. Indeed, all of these common features mirror a shared molecular program, in which Signaling Lymphocytic Activation Molecule Family (SLAMF) receptors and their cytoplasmic binding partner, the adapter signaling lymphocytic activation-associated protein (SAP), play a crucial role. Despite the extensive characterization of SLAMF molecules as a group of cell-surface receptors that regulate and interconnect both innate and adaptive immune cells, their relevance in innate-like lymphocyte ontogeny and physiology has recently taken center stage. Here, we review the current understanding of the roles SLAMF receptors and SAP adaptor molecules play in the biology of innate-like lymphocytes.
    Critical Reviews in Immunology 01/2014; 34(4):263-299.
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    ABSTRACT: Anti-tumor immunotherapy using tumor lysate-based vaccines has made great advances over recent decades. Cancer vaccines aim to elicit adaptive immune responses through various pathways by providing tumor and tumor-associated antigens with an immune stimulant or adjuvant. These anti-tumor vaccines are therefore developed as personalized treatments. Utilizing tumors as a source of vaccine antigens in immunotherapy has demonstrated promising results with minimal toxicity. However, to date, researchers have failed to overcome the overpowering immune suppressive effects within the tumor microenvironment. Immune suppression occurs naturally via multiple mechanisms. These mechanisms serve an important homeostatic role restoring a normal tissue microenvironment following an inflammatory response. Due to these suppressive mechanisms and the inherent heterogeneity of tumors, it is imperative to then elicit and maintain a specific tumoricidal response if vaccine therapy or some other combination of reagents is chosen. In this review, we focus on the historical use of tumors as a source of antigens to elicit a tumoricidal response and the limitations encountered that prevent greater success in immunotherapy. We describe the advantages and disadvantages of various vaccines and their ineffectiveness due to tumor-induced immune suppression.
    Critical Reviews in Immunology 01/2014; 34(5):399-432.
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    ABSTRACT: HLA-DO (H2-O) is a highly conserved nonpolymorphic major histocompatibility complex class II (MHCII) like molecule expressed in B lymphocytes, dendritic cells, and thymic epithelial cells. The biological function of DO has been elusive. Recent studies using site-directed mutagenesis, crystallography, and enzyme kinetics demonstrate that DO functions strictly as an inhibitor rather than modifier of DM function. DO stably binds to DM at the catalytic site to block DM interaction with MHCII. While the new data establish the molecular mechanism of DO function, the reason that professional antigen-presenting cells (APCs) express DO to generate DO-DM complexes that are functionally inactive remains unclear. Despite the finding that DO inhibits DM, antigen presentation by H2-O-/- APCs is inefficient compared to wild-type (WT) APCs, and H2-O-/- mice are partially immunodeficient and spontaneously develop auto-antibodies to nuclear antigens. The results of functional studies raise the question of how an inhibitor of DM enhances antigen presentation and promotes immunity. In this review, we analyze the related findings from previous and recent studies. The integration of the all of the data allows us to propose a model explaining how DO enhances antigen presentation by inhibiting DM function.
    Critical Reviews in Immunology 01/2014; 34(3):215-225.
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    ABSTRACT: IL-10 is an important anti-inflammatory cytokine that plays important roles in controlling inflammatory responses and keeping the immune system in check following activation. Loss of IL-10 function in mice or humans results in the development of inflammatory bowel disease in response to an elevated immune response to the gut flora. IL-10 also acts to prevent excessive inflammation during the course of infection and has been implicated in a variety of autoimmune conditions. In response to inflammatory signals, IL-10 can be produced by a number of immune cells including T cells, B cells, macrophages, and dendritic cells. Distinct mechanisms control the production of IL-10 in these different cells types. In this review, we describe recent studies that have looked at the signaling pathways that regulate IL-10 production in these cells. Given the number of cell types that produce IL-10, it is perhaps not surprising that the in vivo source of IL-10 can vary in different immune models. We also describe how work using conditional IL-10 knockout mice or adoptive transfer of IL-10-deficient cells has begun to further our understanding regarding which specific immune cells are required for IL-10 production in vivo under different conditions.
    Critical Reviews in Immunology 01/2014; 34(4):315-345.
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    ABSTRACT: Monoclonal antibodies constitute a major treatment option for many tumor patients. Due to their specific recognition sites in their constant Fc regions, antibodies are able to trigger antibody-dependent cell-mediated cytotoxicity (ADCC) or complement-dependent cytotoxicity (CDC). While the contribution of ADCC to clinical efficacy has been strengthened by observations that patients with favorable Fcγ receptor polymorphisms display better response rates to therapeutic antibodies, the contribution of CDC to their clinical efficacy remains controversial. In the background of high expression of complement-regulatory proteins on tumor cells as well as of the fact that some therapeutic antibodies lack the capacity to trigger efficient CDC, strategies have been implemented to improve either the capacity of antibodies to initiate the complement cascade or to interfere with tumor cells' resistance mechanisms. Although both strategies have demonstrated therapeutic benefit in vitro and in murine models, CDC-enhanced antibodies−to the best of our knowledge−have not been clinically tested, and evidence for the potential of CDC-optimizing approaches has yet to be generated in humans. Hence, the potency of complement activation and its impact on the clinical efficacy of therapeutic antibodies still remains to be elucidated in clinical trials encompassing novel complement-enhancing molecules.
    Critical Reviews in Immunology 01/2014; 34(3):199-214.
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    ABSTRACT: Influenza infection remains a global threat to human health. Influenza viruses are normally controlled by antibodies specific for the surface glycoproteins hemagglutinin (HA) and neuraminidase (NA). Standard influenza vaccines are aimed at inducing these antibodies, but they must be administered annually and can be rendered ineffective since different strains circulate from year to year and vary considerably in their individual HA and NA profiles. Influenza-specific T cells have been shown to be protective in animal models and typically recognize the more conserved internal influenza proteins. Improving our understanding of influenza-specific T-cell responses, including immunodominance, specific epitope sequences, strain-related epitope variation, host/virus interaction, and the balance between immunity versus immunopathology, will be important to improve future T-cell-based vaccines, which promise broader strain coverage and longer-lasting protection than current standard vaccines.
    Critical Reviews in Immunology 01/2014; 34(1):15-39.
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    ABSTRACT: Activation-induced cell death (AICD) of T cells is a process for regulating the peripheral immune system. The fate of a T cell is controlled by numerous signals derived from various stimuli, such as antigens, cytokines, and chemokines. In healthy humans, overactivated or autoreactive T cells are harmful and are eliminated to maintain the immune system. AICD in T cells by Fas/FasL-mediated apoptosis is triggered by the switch from life to death through several signaling molecules. The control or distribution of Fas or FasL expression largely affects AICD of T cells. Although autoimmune diseases are considered to be induced by multiple factors, an impaired immune system with AICD by Fas/FasL-mediated apoptosis leads to the onset or development of autoimmunity. Based on published reports, this review describes the regulatory mechanisms involved in AICD of T cells by Fas/ FasL-mediated apoptosis and the associations between AICD and autoimmunity in humans and animal models.
    Critical Reviews in Immunology 01/2014; 34(4):301-314.
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    ABSTRACT: Galectin-3 belongs to a family of galectins, evolutionarily conserved glycan binding proteins (lectins) that have recently attracted much attention as modulators in adaptive immune responses. Previously, galectins have been considered lectins that bind only to endogenous "self" glycans. Further, galectins are synthesized and stored in the cytosol, where there are virtually no glycan-containing proteins, raising doubts over the biological significance of their glycan binding capacity. As discussed in this review, with particular emphasis on the role of galectin-3 in the innate immune response against the protozoan parasite Leishmania, several recent studies have suggested that galectin-3 could recognize L. major-specific pathogen-associated molecular pattern and, in parallel, facilitate the infiltration of neutrophils to the infected sites that helps reduce the initial parasite burden once galectin-3 is released as a damage-associated molecular pattern. Thus, while further investigation is necessary, based on the current results, it could be proposed that galectin-3 can hinge two areas of the innate immune recognition system, DAMP and PAMP pathways in the early host responses against various pathogens.
    Critical Reviews in Immunology 01/2014; 34(2):147-175.
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    ABSTRACT: Type 1 diabetes is a T-cell-mediated autoimmune disease in which the insulin-producing cells in the islets of Langerhans are selectively destroyed. Although symptomatic insulin therapy is able to control glucose levels in the blood, many patients do not obtain the desired glycemic control, which increases the risk of diabetic complications. While many immunotherapeutic efforts to intervene in the disease process focus on systemic immune-suppressive therapies, antigen-specific immune modulation represents an attractive alternative. Dendritic cells modulated with 1.25(OH)2 vitamin D3, and dexamethasone (tolerogenic DCs) loaded with islet antigens induce Ag-specific regulatory CD4 T cells (iaTregs), offering a tissue-specific intervention therapy. iaTregs exert their function via linked suppression to diminish effector cells by modulating pro-inflammatory DCs to upregulate inhibitory receptors. In turn, these re-educated mature DCs induce IL-10-producing cells from the naive T-cell pool. Thus, tolerogenic DCs transfer regulatory properties to pro-inflammatory DCs via iaTregs (i.e., infectious tolerance). In this review, we describe the current knowledge regarding regulatory mechanisms of these tolerogenic DCs and the Tregs that they induce, and we propose that cell therapy with human tolerogenic DCs provides new opportunities for immune intervention in patients with autoimmune diseases.
    Critical Reviews in Immunology 01/2013; 33(5):415-434.