Critical Reviews in Immunology Journal Impact Factor & Information

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: 3.70

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 3.698
2013 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

Additional details

5-year impact 3.52
Cited half-life 8.20
Immediacy index 0.30
Eigenfactor 0.00
Article influence 1.25
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
    • Publisher's version/PDF cannot be used
    • Publisher last reviewed on 25/06/2015
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Stress is defined as a state of threatened homeostasis or disharmony that is counteracted by a complex repertoire of physiological and behavioral adaptive responses in order to establish homeostasis. Confronted with a stressful condition, the nervous and immune systems initiate a coping process to maintain homeostasis in the body. Psychological stress, recognized as a public health issue in children and young adults, may be one mechanism to induce and maintain autoimmunity in children. It is necessary to increase our understanding of how psychological stress can affect the immune system at a young age because autoimmune diseases, especially type 1 diabetes, are alarmingly common in children. Psychological stress may be involved in other autoimmune diseases, such as celiac disease, systemic lupus erythematosus, and juvenile idiopathic arthritis, that frequently occur in children as well. This review summarizes the studies attempting to evaluate the link between psychological stress and autoimmune response in children. A number of them have observed that the autoimmune disease itself causes psychological stress. We are far from fully understanding how long-term psychological stress is linked to autoimmune response in children with a high risk of, or already diagnosed, autoimmune disease.
    Critical Reviews in Immunology 09/2015; 35(2). DOI:10.1615/CritRevImmunol.2015013255
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    ABSTRACT: Numerous studies have shown that TH17 cells and their signature cytokine IL-17A are critical to host defense against various bacterial and fungal infections. The protective responses mediated by TH17 cells and IL-17A include the recruitment of neutrophils, release of antimicrobial peptides and chemokines, and enhanced tight junction of epithelial cells. Due to the importance of TH17 cells in infections, efforts have been made to develop TH17-based vaccines. The goal of vaccination is to establish a protective immunological memory. Most currently approved vaccines are antibody-based and have limited protection against stereotypically different strains. Studies show that T-cell-based vaccines may overcome this limitation and protect hosts against infection of different strains. Two main strategies are used to develop TH17 vaccines: identification of TH17-specific antigens and TH17-skewing adjuvants. Studies have revealed that cholera toxin (CT) induces a potent Th17 response following vaccination. Antigen vaccination along with CT induces a robust TH17 response, which is sometimes accompanied by TH1 responses. Due to the toxicity of CT, it is hard to apply CT in a clinical setting. Thus, understanding how CT modulates TH17 responses may lead to the development of successful TH17-based vaccines.
    Critical Reviews in Immunology 09/2015; 35(2). DOI:10.1615/CritRevImmunol.2015012295
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    ABSTRACT: Lipocalin-2 (LCN2), a secretory protein, regulates diverse cellular processes such as cell death/survival, cell migration/invasion, cell differentiation, iron delivery, inflammation, insulin resistance, and tissue regeneration. Recently, we reported that LCN2 is secreted by brain astrocytes under inflammatory conditions and that it promotes apoptosis, morphological changes, and migration in astrocytes both in vitro and in vivo. Activated astrocytes release LCN2 not only to induce the morphological transformation associated with reactive astrocytosis, but also to promote their own death. Under inflammatory conditions, activated astrocytes also show functional dichotomy similar to the M1/M2 phenotypes of microglia and macrophages. LCN2 is thought to be a chemokine inducer and an autocrine promoter of the classical proinflammatory activation of astrocytes. This article summarizes the current knowledge regarding the role of astrocyte-derived LCN2 as a proinflammatory mediator in the central nervous system and discusses LCN2’s role in neuroinflammatory disorders.
    Critical Reviews in Immunology 06/2015; 35(1):77-84.
  • Critical Reviews in Immunology 04/2015; 35(1):77-84. DOI:10.1615/CritRevImmunol.2015012127
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    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 03/2015; 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 03/2015; 35(1):33-48. DOI:10.1615/CritRevImmunol.2015012207
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    ABSTRACT: Development and central tolerance of T lymphocytes in the thymus requires both TCR signals and collaboration with signals generated through costimulatory molecule interactions. In this review, we discuss the importance of CD28-CD80/86 and CD40-CD40L costimulatory interactions in promoting normal thymic development. This discussion includes roles in the generation of a normal thymic medulla, in the development of specific T-cells subsets, including iNKT and T regulatory cells, and in the generation of a tolerant mature T-cell repertoire. We discuss recent contributions to the understanding of CD28-CD80/86 and CD40-CD40L costimulatory interactions in thymic development, and we highlight the ways in which the many important roles mediated by these interactions collaborate to promote normal thymic development.
    Critical Reviews in Immunology 03/2015; 35(1):59-76. DOI:10.1615/CritRevImmunol.2015012501
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    ABSTRACT: T regulatory cells (Tregs) comprise the cardinal mechanism of peripheral immune tolerance by modulating the function of virtually each immune cell. Given that atherosclerosis is a chronic inflammation of the arterial wall, certain components of the immune system have been proven to have a central role in its pathogenesis. Consequently, various clinical and experimental studies have been conducted to elucidate the role of Tregs in suppressing this immune-mediated inflammation. In this review, current experimental and clinical knowledge on the role of Tregs in the atherogenic process is presented after a short introduction to their generation and function. Based on these data, Treg-targeted therapeutic approaches are discussed in regard to their potential for clinical application.
    Critical Reviews in Immunology 11/2014; 34(5):389-97. DOI:10.1615/CritRevImmunol.2014010802
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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 06/2014; 34(4):301-314. DOI:10.1615/CritRevImmunol.2014009988
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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 06/2014; 34(2):147-175. DOI:10.1615/CritRevImmunol.2014010154
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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 06/2014; 34(3):241-261. DOI:10.1615/CritRevImmunol.2014010267
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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 06/2014; 34(3):215-225. DOI:10.1615/CritRevImmunol.2014009999