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

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Autoimmune diseases (ADs), or autoinflammatoiy diseases, are growing in complexity as diagnoses improve and many factors escalate disease risk. Considerable genetic similarity is found among ADs, and they are frequently associated with major histocompatibility complex (MHC) genes. However, a given disease may be associated with more than one human leukocyte antigen (HLA) allotype, and a given HLA may be associated with more than one AD. The associations of non-MHC genes with AD present an additional problem, and the situation is further complicated by the role that other factors, such as age, diet, therapeutic drugs, and regional influences, play in disease. This review discusses some of the genetics and biochemistry of HLA-linked AD and inflammation, covering some of the best-studied examples and summarizing indicators for class I- and II-mediated disease. However, the scope of this review limits a detailed discussion of all known ADs.
    Critical Reviews in Immunology 11/2015; 35(3):203-251.
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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

  • Critical Reviews in Immunology 01/2015; DOI:10.1615/CritRevImmunol.2015014925
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    ABSTRACT: Dengue virus (DENV), the most prevalent mosquito-borne viral diseases in humans worldwide, causes dengue fever, a mild form of the disease, as well as dengue hemorrhagic fever/dengue shock syndrome, a more severe form which can be life-threatening. The four serotypes of DENV (DENV1-4) are positive-sense, single stranded RNA virus belonging to the Flaviviridae family and are transmitted by Aedes aegypti and Aedes albopictus mosquitoes. Together, they are estimated to cause almost 100 million symptomatic cases, 2.1 million cases of dengue hemorrhagic fever/dengue shock syndrome, and 21,000 deaths per year worldwide. There are currently no effective vaccines or antiviral treatment for DENV. Innate immune defenses play a key role in controlling DENV infection in the early stages. Herein we review the innate antiviral immunity against DENV by delineating the intracellular mechanisms of the immune response and the evasion mechanisms evolved by the virus. A better understanding of the innate immune response will impact the development of novel animal models, antiviral drugs as well as potential targeted adjuvants for DENV vaccines.
    Critical Reviews in Immunology 01/2015; 35(3). DOI:10.1615/CritRevImmunol.2015014251
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    ABSTRACT: Acute respiratory tract infections (ARTIs) are the major cause of child mortality worldwide. The human metapneumovirus (hMPV) is one of the leading causes of child hospitalizations due to pneumonia. The adaptive immune response generated by the host against hMPV is usually inefficient at protecting from reinfections, which is repeat throughout life, from childhood to old age. Despite considerable research efforts, to date there are no licensed vaccines to prevent respiratory disease caused by hMPV infection. In this article we review current vaccine strategies tested in animal models and the implication of such studies in understanding the different immune cell populations that contribute to hMPV clearance and the prevention and resolution of lung inflammation upon exposure to the virus.
    Critical Reviews in Immunology 01/2015; 35(3). DOI:10.1615/CritRevImmunol.2015013844
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    ABSTRACT: The fight between a human host and a bacterial pathogen is highly complicated; each party tries to outshine the other in the race for survival. In humans, the innate immune system—in particular the complement system—functions as the first line of defence against invading pathogens. During the course of evolution, however, pathogens, in order to survive and perpetuate within a host, developed multiple strategies to counteract the host complement system and to colonize. One such pathogen is Streptococcus pneumoniae (pneumococcus), a gram-positive bacterial pathogen often commensal in the human respiratory tract. Depending on the host’s susceptibility, pneumococci can transform into an infectious agent, disseminating within the human host and causing mild to life-threatening diseases. This transition from commensal to infectious agent is a highly complex process, and understanding of this mechanism is essential in controlling the pathogenicity of pneumococci. Using its intricate arsenal of weapons, such as surface-presenting adhesins as well as recruitment of host factor, pneumococci successfully colonize the host, a prerequisite for establishing infection. This review describes C1q, the first subunit of the classical complement pathway, and its role in pneumococcus–host interactions, whereby pneumococci exploit C1q as a molecular bridge facilitating host cellular adherence and invasion, a function not akin to the role of C1q in the defence mechanism.
    Critical Reviews in Immunology 01/2015; 35(3). DOI:10.1615/CritRevImmunol.2015012177

  • Critical Reviews in Immunology 01/2015; DOI:10.1615/CritRevImmunol.2015014417

  • Critical Reviews in Immunology 01/2015; DOI:10.1615/CritRevImmunol.2015015495

  • Critical Reviews in Immunology 01/2015; DOI:10.1615/CritRevImmunol.2015015461
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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