Critical Reviews in Immunology (CRIT REV IMMUNOL)

Publisher: Begell House

Journal 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.

Current impact factor: 3.89

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 3.889
2012 Impact Factor 3.383
2011 Impact Factor 3.317
2010 Impact Factor 3.857
2009 Impact Factor 2.625
2008 Impact Factor 3.241
2007 Impact Factor 4.058
2006 Impact Factor 3.938
2005 Impact Factor 3.214
2004 Impact Factor 3.595
2003 Impact Factor 3.113
2002 Impact Factor 3.019
2001 Impact Factor 6.07
2000 Impact Factor 6.981
1999 Impact Factor 5.726
1998 Impact Factor 5.955
1997 Impact Factor 3.967
1996 Impact Factor 3
1995 Impact Factor 4.333
1994 Impact Factor 6
1993 Impact Factor 3.931
1992 Impact Factor 4.774

Impact factor over time

Impact factor
Year

Additional details

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
    • NIH Authors can deposit in PubMed Central for public release after 12 month embargo
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Neuroinflammation contributes to neuronal deficits in neurodegenerative CNS (central nervous system) autoimmune diseases, such as multiple sclerosis and uveitis. The major goal of most treatment modalities for CNS autoimmune diseases is to limit inflammatory responses in the CNS; immune-suppressive drugs are the therapy of choice. However, lifelong immunosuppression increases the occurrence of infections, nephrotoxicity, malignancies, cataractogenesis, and glaucoma, which can greatly impair quality of life for the patient. Biologics that target pathogenic T cells is an alternative approach that is gaining wide acceptance as indicated by the popularity of a variety of Food and Drug Administration (FDA)-approved anti-inflammatory compounds and humanized antibodies such as Zenapax, Etanercept, Remicade, anti-ICAM, rapamycin, or tacrolimus. B cells are also potential therapeutic targets because they provide costimulatory signals that activate pathogenic T cells and secrete cytokines that promote autoimmune pathology. B cells also produce autoreactive antibodies implicated in several organ-specific and systemic autoimmune diseases including lupus erythematosus, Graves' disease, and Hashimoto's thyroiditis. On the other hand, recent studies have led to the discovery of several regulatory B-cell (Breg) populations that suppress immune responses and autoimmune diseases. In this review, we present a brief overview of Breg phenotypes and in particular, the newly discovered IL35-producing regulatory B cell (i35-Breg). We discuss the critical roles played by i35-Bregs in regulating autoimmune diseases and the potential use of adoptive Breg therapy in CNS autoimmune diseases.
    Critical Reviews in Immunology 01/2015; 35(1):49-57. DOI:10.1615/CritRevImmunol.2015012558
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    ABSTRACT: Natural killer T (NKT) cells are αβ T cells that express a semi-invariant T-cell receptor (TCR) along with natural killer (NK) cell markers and have an innate cell-like ability to produce a myriad of cytokines very quickly upon antigen exposure and subsequent activation. These cells are diverted from conventional single positive (SP) T-cell fate at the double positive (DP) stage, where TCR-mediated recognition of a lipid antigen presented on a CD1d molecule promotes their selection into the NKT lineage. Although many key regulatory molecules have been shown to play important roles in the development of NKT cells, the mechanism of lineage specification and acquisition of effector functions in these cells still remain to be fully addressed. In this review, we specifically discuss the role of a family of class-I helix-loop-helix proteins known as E proteins, and their antagonists Id proteins in NKT celldevelopment. Recent work has shown that these proteins play key roles in invariant NKT (iNKT) development, from the invariant TCR rearrangement to terminal differentiation and maturation. Elucidating these roles provides an opportunity to uncover the transcriptional network that separates NKT cells from concurrently developed conventional αβ T cells.
    Critical Reviews in Immunology 01/2015; 35(1):33-48. DOI:10.1615/CritRevImmunol.2015012207
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    ABSTRACT: Dynamic reorganization of the cortical cytoskeleton is essential for numerous cellular processes, including B- and T-cell activation and migration. The ezrin-radixin-moesin (ERM) family of proteins plays structural and regulatory roles in the rearrangement of plasma membrane flexibility and protrusions through its members' reversible interaction with cortical actin filaments and the plasma membrane. Recent studies demonstrated that ERM proteins not only are involved in cytoskeletal organization but also offer a platform for the transmission of signals in response to a variety of extracellular stimuli through their ability to cross-link transmembrane receptors with downstream signaling components. In this review, we summarize present knowledge relating to ERMs and recent progress made toward elucidating a novel role for them in the regulation of B-cell function in health and disease.
    Critical Reviews in Immunology 01/2015; 35(1). DOI:10.1615/CritRevImmunol.2015012327
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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. DOI:10.1615/CritRevImmunol.2014010267
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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. DOI:10.1615/CritRevImmunol.2013008686
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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. DOI:10.1615/CritRevImmunol.2013006833
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    ABSTRACT: B cells can be activated by cognate antigen, anti-B-cell receptor antibody, complement receptors, or polyclonal stimulators like lipopolysaccharide; the overall result is a large shift in RNA processing to the secretory-specific form of immunoglobulin (Ig) heavy chain mRNA and an upregulation of Igh mRNA amounts. Associated with this shift is the large-scale induction of Ig protein synthesis and the unfolded protein response to accommodate the massive quantity of secretory Ig that results. Stimulation to secretion also produces major structural accommodations and stress, with extensive generation of endoplasmic reticulum and Golgi as part of the cellular architecture. Reactive oxygen species can lead to either activation or apoptosis based on context and the high or low oxygen tension surrounding the cells. Transcription elongation factor ELL2 plays an important role in the induction of Ig secretory mRNA production, the unfolded protein response, and gene expression during hypoxia. After antigen stimulation, activated B cells from either the marginal zones or follicles can produce short-lived antibody secreting cells; it is not clear whether cells from both locations can become long-lived plasma cells. Autophagy is necessary for plasma cell long-term survival through the elimination of some of the accumulated damage to the ER from producing so much protein. Survival signals from the bone marrow stromal cells also contribute to plasma cell longevity, with BCMA serving a potentially unique survival role. Integrating the various information pathways converging on the plasma cell is crucial to the development of their long-lived, productive immune response.
    Critical Reviews in Immunology 01/2014; 34(2014 Issue 6):481-499. DOI:10.1615/CritRevImmunol.2014012168
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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. DOI:10.1615/CritRevImmunol.2014009982
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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. DOI:10.1615/CritRevImmunol.2014010088
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    ABSTRACT: Mouse strains are frequently used to model human disease states, to test the efficiency of drugs and therapeutic principles. However, the direct translation of murine experimental data to human pathological events often fails due to sufficient differences in the organization of the immune system of both species. Here we give a short overview of the principle differences between mice and humans in defense strategies against pathogens and mechanisms involved in response to pathogenic microorganisms and other activators of the immune system. While in human blood mechanisms of immune resistance are highly prevailed, tolerance mechanisms dominate for the defense against pathogenic microorganisms in mouse blood. Further on, species-related differences of immune cells mainly involved in innate immune response as well as differences to maintain oxidative homeostasis are also considered. A number of disease scenarios in mice are critically reflected for their suitability to serve as a model for human pathologies. Due to setbacks in these studies, novel mouse models were created to bridge the immune system of both species: humanized mice. Accordingly, a special section of this review is devoted to new results applying humanized mouse models taking limitations and prospects into account.
    Critical Reviews in Immunology 01/2014; 34(5):433-54. DOI:10.1615/CritRevImmunol.2014011600
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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. DOI:10.1615/CritRevImmunol.2014010538
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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. DOI:10.1615/CritRevImmunol.2014010062
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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. DOI:10.1615/CritRevImmunol.2014011577
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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. DOI:10.1615/CritRevImmunol.2014009761