Nature reviews. Immunology (NAT REV IMMUNOL)

Publisher: Nature Publishing Group

Journal description

Current impact factor: 33.84

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 33.836
2012 Impact Factor 33.129
2011 Impact Factor 33.287
2010 Impact Factor 35.196
2009 Impact Factor 32.245
2008 Impact Factor 30.006
2007 Impact Factor 28.3
2006 Impact Factor 28.697
2005 Impact Factor 30.458
2004 Impact Factor 32.695
2003 Impact Factor 26.957
2002 Impact Factor 14.059

Impact factor over time

Impact factor

Additional details

5-year impact 35.85
Cited half-life 5.50
Immediacy index 4.83
Eigenfactor 0.11
Article influence 16.90
Website Nature Reviews Immunology website
Other titles Immunology
ISSN 1474-1733
OCLC 48623854
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Nature Publishing Group

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 6 months embargo
  • Conditions
    • Authors retain copyright
    • Author's pre-print on arXiv or bioRXiv
    • Author's post-print on author's personal website, institutional repository, PubMed Central or funding body's archive
    • Published source must be acknowledged
    • Must link to publisher version with DOI
    • Publisher's version/PDF cannot be used
  • Classification
    ​ yellow

Publications in this journal

  • Nature reviews. Immunology 03/2015; DOI:10.1038/nri3835
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    ABSTRACT: Improved treatments are needed for nearly all forms of Mycobacterium tuberculosis infection. Adjunctive host-directed therapies have the potential to shorten tuberculosis treatment duration, prevent resistance and reduce lung injury by promoting autophagy, antimicrobial peptide production and other macrophage effector mechanisms, as well as by modifying specific mechanisms that cause lung inflammation and matrix destruction. The range of candidates is broad, including several agents approved for other clinical indications that are ready for evaluation in Phase II clinical trials. The promise of new and existing host-directed therapies that could accelerate response and improve tuberculosis treatment outcomes is discussed in this Opinion article.
    Nature reviews. Immunology 03/2015; DOI:10.1038/nri3813
  • Nature reviews. Immunology 02/2015; DOI:10.1038/nri3828
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    ABSTRACT: The regulation of antibody production is linked to the generation and maintenance of plasmablasts and plasma cells from their B cell precursors. Plasmablasts are the rapidly produced and short-lived effector cells of the early antibody response, whereas plasma cells are the long-lived mediators of lasting humoral immunity. An extraordinary number of control mechanisms, at both the cellular and molecular levels, underlie the regulation of this essential arm of the immune response. Despite this complexity, the terminal differentiation of B cells can be described as a simple probabilistic process that is governed by a central gene-regulatory network and modified by environmental stimuli.
    Nature reviews. Immunology 02/2015; DOI:10.1038/nri3795
  • Nature reviews. Immunology 02/2015; DOI:10.1038/nri3829
  • Nature reviews. Immunology 02/2015; DOI:10.1038/nri3827
  • Nature reviews. Immunology 02/2015; DOI:10.1038/nri3826
  • Nature reviews. Immunology 02/2015; DOI:10.1038/nri3825
  • Nature reviews. Immunology 02/2015; DOI:10.1038/nri3822
  • Nature reviews. Immunology 02/2015; DOI:10.1038/nri3821
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    ABSTRACT: Humoral immunity depends on the germinal centre (GC) reaction during which somatically mutated high-affinity memory B cells and plasma cells are generated. Recent studies have uncovered crucial cues that are required for the formation and the maintenance of GCs and for the selection of high-affinity antibody mutants. In addition, it is now clear that these events are promoted by the dynamic movements of cells within and between GCs. These findings have resolved the complexities of the GC reaction in greater detail than ever before. This Review focuses on these recent advances and discusses their implications for the establishment of humoral immunity.
    Nature reviews. Immunology 02/2015; DOI:10.1038/nri3804
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    ABSTRACT: The separate development of functionally intertwined lineages of lymphocytes known as B cells and T cells is now recognized as a fundamental organizing principle of the adaptive immune system in all vertebrates. Immunologists strive to define the different sublineages of the clonally diverse B cells and T cells, how they interact with each other and how they interact with innate lymphoid cells and other elements of the innate immune system to counter infections, cancer and the development of autoimmune and inflammatory diseases. On the 50th anniversary of the recognition of B cells as a discrete cell lineage, this Timeline article recounts some of the milestones marking the development of the concept that B cells are a functionally and developmentally distinct arm of the adaptive immune system.
    Nature reviews. Immunology 02/2015; DOI:10.1038/nri3801
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    ABSTRACT: Metastatic disease is the major cause of death from cancer, and immunotherapy and chemotherapy have had limited success in reversing its progression. Data from mouse models suggest that the recruitment of immunosuppressive cells to tumours protects metastatic cancer cells from surveillance by killer cells, which nullifies the effects of immunotherapy and thus establishes metastasis. Furthermore, in most cases, tumour-infiltrating immune cells differentiate into cells that promote each step of the metastatic cascade and thus are novel targets for therapy. In this Review, we describe how tumour-infiltrating immune cells contribute to the metastatic cascade and we discuss potential therapeutic strategies to target these cells.
    Nature reviews. Immunology 01/2015; 15(2):73-86. DOI:10.1038/nri3789
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    ABSTRACT: Type I interferons (IFNs) have diverse effects on innate and adaptive immune cells during infection with viruses, bacteria, parasites and fungi, directly and/or indirectly through the induction of other mediators. Type I IFNs are important for host defence against viruses. However, recently, they have been shown to cause immunopathology in some acute viral infections, such as influenza virus infection. Conversely, they can lead to immunosuppression during chronic viral infections, such as lymphocytic choriomeningitis virus infection. During bacterial infections, low levels of type I IFNs may be required at an early stage, to initiate cell-mediated immune responses. High concentrations of type I IFNs may block B cell responses or lead to the production of immunosuppressive molecules, and such concentrations also reduce the responsiveness of macrophages to activation by IFNγ, as has been shown for infections with Listeria monocytogenes and Mycobacterium tuberculosis. Recent studies in experimental models of tuberculosis have demonstrated that prostaglandin E2 and interleukin-1 inhibit type I IFN expression and its downstream effects, demonstrating that a cross-regulatory network of cytokines operates during infectious diseases to provide protection with minimum damage to the host.
    Nature reviews. Immunology 01/2015; 15(2):87-103. DOI:10.1038/nri3787
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    ABSTRACT: Hypercholesterolaemia leads to cholesterol accumulation in macrophages and other immune cells, which promotes inflammatory responses, including augmentation of Toll-like receptor (TLR) signalling, inflammasome activation, and the production of monocytes and neutrophils in the bone marrow and spleen. On a cellular level, activation of TLR signalling leads to decreased cholesterol efflux, which results in further cholesterol accumulation and the amplification of inflammatory responses. Although cholesterol accumulation through the promotion of inflammatory responses probably has beneficial effects in the response to infections, it worsens diseases that are associated with chronic metabolic inflammation, including atherosclerosis and obesity. Therapeutic interventions such as increased production or infusion of high-density lipoproteins may sever the links between cholesterol accumulation and inflammation, and have beneficial effects in patients with metabolic diseases.
    Nature reviews. Immunology 01/2015; 15(2):104-16. DOI:10.1038/nri3793
  • Nature reviews. Immunology 01/2015; 15(2):69. DOI:10.1038/nri3816
  • Nature reviews. Immunology 01/2015; 15(2):69. DOI:10.1038/nri3817
  • Nature reviews. Immunology 01/2015; 15(2):68-9. DOI:10.1038/nri3811
  • Nature reviews. Immunology 01/2015; 15(2):69. DOI:10.1038/nri3815
  • Nature reviews. Immunology 01/2015; 15(2):70-1. DOI:10.1038/nri3812