Critical Reviews in Immunology (CRIT REV IMMUNOL )

Publisher: Begell House

Description

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.

  • Impact factor
    3.38
    Show impact factor history
     
    Impact factor
  • 5-year impact
    3.22
  • Cited half-life
    7.30
  • Immediacy index
    0.44
  • Eigenfactor
    0.00
  • Article influence
    1.10
  • Website
    Critical Reviews in Immunology website
  • Other titles
    Critical reviews in immunology, Chemical Rubber Company critical reviews in immunology, CRC critical reviews in immunology
  • ISSN
    1040-8401
  • OCLC
    18553639
  • Material type
    Periodical
  • Document type
    Journal / Magazine / Newspaper

Publisher details

Begell House

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author cannot archive a post-print version
  • Conditions
    • Deposit in institutional repositories is not allowed
    • Policy under discussion [21/04/08]
  • Classification
    ​ white

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.
    Critical Reviews in Immunology 04/2014; 34(2):121-146.
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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: 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: 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: 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: A balanced immune response to a viral pathogen leads to clearance of the virus while limiting immune mediated pathology. Control of this process occurs at all stages of the immune response, including during the induction of an antiviral response, clearance of virally infected cells, and the resolution of this response. Regulation of antiviral immune response is further modified when the immune system fails to clear the pathogen and by the nature of chronic infection itself. A number of processes have been implicated in the regulation of antiviral immune responses, such as the limitation of viral antigen load by interferons, apoptosis through cytokine withdrawal or Fas-mediated killing, and control of these responses by regulatory T cells. This review addresses several of these mechanisms.
    Critical Reviews in Immunology 01/2013; 33(6):477-488.
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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.
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    ABSTRACT: Allergic diseases are an increasing health concern, particularly in the developed world. The standard clinical approach to treatment of allergic disease focuses on allergen avoidance and symptom control but does little to address the underlying Th2 bias of disease. Specific immunotherapy (SIT) consisting of controlled administration of allergen, however, has been demonstrated to successfully induce desensitization and tolerance in an antigen-specific manner for a variety of Th2-mediated diseases. This review focuses on the mechanisms by which current SIT approaches induce tolerance as well as discussing attempts to modify the safety and efficacy of SIT. These refinements focus on three major aspects of SIT: the route of antigen administration, modification of the antigen to remove allergenic epitopes and reduce adverse events and choice of adjuvant used to induce tolerance and/or immune deviation from Th2 to Th1 and regulatory T-cell (Treg) phenotypes. Synthesis of these recent developments in SIT provides considerable promise for more robust therapies with improved safety profiles to improve resolution of allergic disease and its associated costs.
    Critical Reviews in Immunology 01/2013; 33(5):389-414.
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    ABSTRACT: Chronic infectious diseases such as HIV, HBV, and HCV, among others, cause severe morbidity and mortality globally. Progressive decline in CD8 functionality, survival, and proliferative potential-a phenomenon referred to as CD8 exhaustion-is believed to be responsible for poor pathogen control in chronic infectious diseases. While the role of negative inhibitory receptors such as PD-1 in augmenting CD8 exhaustion has been extensively studied, the role of positive costimulatory receptors remains poorly understood. In this review, we discuss how one such costimulatory pathway, CD40-CD40L, regulates CD8 dysfunction and rescue. While the significance of this pathway has been extensively investigated in models of autoimmunity, acute infectious diseases, and tumor models, the role played by CD40-CD40L in regulating CD8 exhaustion in chronic infectious diseases is just beginning to be understood. Considering that monotherapy with blocking antibodies targeting inhibitory PD-1-PD-L1 pathway is only partially effective at ameliorating CD8 exhaustion and that humanized CD40 agonist antibodies are currently available, a better understanding of the role of the CD40-CD40L pathway in chronic infectious diseases will pave the way for the development of more robust immunotherapeutic and prophylactic vaccination strategies.
    Critical Reviews in Immunology 01/2013; 33(4):361-78.
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    ABSTRACT: Regulation of immune responses and control of autoimmunity depend on layers of checkpoints, cell-cell interactions, and soluble mediators, both during lymphocyte development and in the course of immune responses. With the definition and study of multiple distinct T-cell subsets, it is now apparent that, while specialized regulatory T cells (Tregs) have essential roles in immune homeostasis, important regulatory interactions also occur between the known effector Th subsets such as Тh1, Th2 and Th17. In this review, we discuss the regulatory effects of the Th2 cell cytokine interleukin 4 (IL-4) on Тh17 cell function, and we highlight emerging data, which indicate the importance of this interaction in both animal model systems and human disease.
    Critical Reviews in Immunology 01/2013; 33(5):379-387.
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    ABSTRACT: Numerous studies have documented abnormal expression and activation of the Ron receptor tyrosine kinase in a variety of human malignancies. Here we review the literature regarding the molecular mechanisms governing Ron regulation, the biological functions of Ron, the effect of Ron on cancer development, and potential therapeutic implications. In epithelial cells, activation of Ron by its ligand, macrophage stimulating protein, mediates a number of biological events including cell growth, motility, and epithelial to mesenchymal transition. Overexpression and/or activation of Ron has been implicated in the progression and metastasis of diverse epithelial cancers, where it plays a causal role in tumor development by promoting growth, survival, and motility of tumor cells. As a crucial regulator of inflammation, Ron inhibits classic macrophage activation and promotes alternative activation of macrophages, resulting in the resolution of inflammation and tissue repair. In addition, Ron alleviates antitumor immunity by promoting the alternative activation of tumor-associated macrophages, and Ron expression in the tumor microenvironment promotes the outgrowth of metastatic colonies. Hence, Ron is a promising therapeutic target for the treatment of epithelial cancers.
    Critical Reviews in Immunology 01/2013; 33(6):549-574.
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    ABSTRACT: Muller cells are the predominant glial cell type in the retina and have a unique anatomy, with processes that span the entire retinal thickness. Although extensive morphological and physiological studies of Muller glia have been performed, much less is known about their role in retinal innate immunity, specifically in infectious endophthalmitis. They were found to express toll-like receptors (TLRs), a major family of pattern recognition receptors that mediate innate responses and provide an important mechanism by which Muller glia are able to sense both pathogen- and host-derived ligands in the vitreous and the retina. An increasing body of evidence suggests that TLR-signaling mediates beneficial effects in the retina via production of proinflammatory cytokines/chemokines, antimicrobial peptides, and neuroprotective growth factors to restore tissue homeostasis. In this review, we discussed retinal innate immunity in general with emphasis on the role of Muller glia in initiating retinal innate defense.
    Critical Reviews in Immunology 01/2013; 33(2):119-35.
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    ABSTRACT: MicroRNAs (miRNA) are a class of small non-coding RNAs that constitute an essential and evolutionarily conserved mechanism for post-transcriptional gene regulation. Multiple miRNAs have been described to play key roles in T-lymphocyte development, differentiation, and function. In this review, we highlight the current literature regarding the differential expression of miRNAs in various models of murine and human T-cell biology. We emphasize mechanistic understandings of miRNA regulation of thymocyte development, T-cell activation, and differentiation into effector and memory subsets. We describe the participation of miRNAs in complex regulatory circuits shaping T-cell proteomes in a context-dependent manner. It is striking that some miRNAs regulate multiple processes, while others only appear in limited functional contexts. It is also evident that the expression and function of specific miRNAs can differ between murine and human systems. Ultimately, it is not always correct to simplify the complex events of T-cell biology into a model driven by only one or two master regulator miRNAs. In reality, T-cell activation and differentiation involve the expression of multiple miRNAs with many mRNA targets; thus, the true extent of miRNA regulation of T-cell biology is likely far more vast than currently appreciated.
    Critical Reviews in Immunology 01/2013; 33(5):435-476.
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    ABSTRACT: Killer Immunoglobulin-like Receptors (KIR) are a family of receptors expressed on natural killer (NK) and T-cell subsets. KIR3DL1 is a highly polymorphic receptor that binds to groups of HLAA and HLA-B allotypes that express the Bw4 epitope. The variation in KIR3DL1 allotypes manifests at a number of levels. Most dramatically, a common allelic variant encodes an activating rather than an inhibitory receptor (KIR3DS1). In addition, sequence variants can affect both the frequency of expression within the NK cell population and the intensity of expression on a given cell. KIR3DL1 polymorphism also influences the interaction with HLA-Bw4 molecules, due to contacts with the HLA molecule itself and sensitivity to the presented peptide. A body of evidence from genetic association studies supports the biological significance not only of the interaction of KIR3DL1 with HLA-Bw4 but also the functional variation seen with different KIR3DL1 and HLA allotypes. In this review, we discuss our current understanding of KIR3DL1 function and our recent insights from the structure of the KIR3DL1 in complex with HLA. In addition, we will summarize our current understanding of KIR3DS1, including its ligand specificity and its role in immune responses.
    Critical Reviews in Immunology 01/2013; 33(3):203-18.
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    ABSTRACT: Type 1 diabetes is a prototypic, organ-specific autoimmune disease. Diverse antigen-specific immunotherapy using insulin or glutamic acid decarboxylase peptides and other immunotherapies, such as antibodies, fusion proteins, cytokines, regulatory T cells, small-molecule inhibitors, nonspecific immune modulators, or dietary modifications, have been attempted in human type 1 diabetes. Some of these immunotherapies delay the onset of diabetes or reduce insulin requirements or blood glucose level in patients with established type 1 diabetes. However, most of these immunotherapies failed to induce complete remission of established type 1 diabetes, which could be due to 1) technical difficulties in the achievement of immune tolerance to diabetic autoantigens or in the inhibition of autoimmune responses to those antigens that can be applied to human patients without significant adverse effects, and 2) markedly reduced β-cell mass at the time of disease onset that should be replenished. This review focuses on the immunological aspects of the disease and its treatment, and data from previous or ongoing human clinical trials using immune-logical measures, and recent results from immunological studies employing animal models are discussed.
    Critical Reviews in Immunology 01/2013; 33(3):245-81.
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    ABSTRACT: The persistence of chronic immune activation and oxidative stress in human immunodeficiency virus (HIV)-infected, antiretroviral drug-treated individuals are major obstacles to fully preventing HIV disease progression. The immune modulator and antioxidant dimethyl fumarate (DMF) is effective in treating immune-mediated diseases and it also has potential applications to limiting HIV disease progression. Among the relevant effects of DMF and its active metabolite monomethyl fumarate (MMF) are induction of a Th1 to Th2 lymphocyte shift, inhibition of pro-inflammatory cytokine signaling, inhibition of NF-κB nuclear translocation, inhibition of dendritic cell maturation, suppression of lymphocyte and endothelial cell adhesion molecule expression, and induction of the Nrf2-dependent antioxidant response element (ARE) and effector genes. Associated with these effects are reduced lymphocyte and monocyte infiltration into psoriatic skin lesions in humans and immune-mediated demyelinating brain lesions in rodents, which confirms potent systemic and central nervous system (CNS) effects. In addition, DMF and MMF limit HIV infection in macrophages in vitro, albeit by unknown mechanisms. Finally, DMF and MMF also suppress neurotoxin production from HIV-infected macrophages, which drives CNS neurodegeneration. Thus, DMF might protect against systemic and CNS complications in HIV infection through its effective suppression of immune activation, oxidative stress, HIV replication, and macrophage-associated neuronal injury.
    Critical Reviews in Immunology 01/2013; 33(4):307-59.
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    ABSTRACT: Caspase recruitment domain-containing membrane-associated guanylate kinase protein-1 (CARMA1), a member of the membrane associated guanylate kinase (MAGUK) family of kinases, is essential for T lymphocyte activation and proliferation via T-cell receptor (TCR) mediated NF-κB activation. Recent studies suggest a broader role for CARMA1 regulating other T-cell functions as well as a role in non-TCR-mediated signaling pathways important for lymphocyte development and functions. In addition, CARMA1 has been shown to be an important component in the pathogenesis of several human diseases. Thus, comprehensively defining its mechanisms of action and regulation could reveal novel therapeutic targets for T-cell-mediated diseases and lymphoproliferative disorders.
    Critical Reviews in Immunology 01/2013; 33(3):219-43.

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