Immunology Letters Journal Impact Factor & Information

Publisher: Elsevier

Journal description

Immunology Letters provides a vehicle for the speedy publication of full-length and short articles, Rapid Notes, (mini)Reviews and Letters to the Editor addressing all aspects of molecular and cellular immunology. The essential criteria for publication will be clarity, experimental soundness and novelty. Results contradictory to current accepted thinking or ideas divergent from actual dogmas will be considered for publication provided that they are based on solid experimental findings. Preference will be given to papers of immediate importance to other investigators, either by their experimental data, new ideas or new methodology. Scientific correspondence to the Editor-in-Chief related to the published papers may also be accepted provided that they are short and scientifically relevant to the papers mentioned, in order to provide a continuing forum for discussion. Within a reference section, new mRNA sequences with unknown function, expressed sequence tags with tissue distribution and novel monoclonal antibody descriptions are considered for publication.

Current impact factor: 2.51

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.512
2013 Impact Factor 2.367
2012 Impact Factor 2.337
2011 Impact Factor 2.526
2010 Impact Factor 2.511
2009 Impact Factor 2.906
2008 Impact Factor 2.858
2007 Impact Factor 2.628
2006 Impact Factor 2.352
2005 Impact Factor 2.301
2004 Impact Factor 2.136
2003 Impact Factor 1.71
2002 Impact Factor 1.847
2001 Impact Factor 2.009
2000 Impact Factor 1.546
1999 Impact Factor 1.494
1998 Impact Factor 1.485
1997 Impact Factor 1.096
1996 Impact Factor 1.255
1995 Impact Factor 1.241
1994 Impact Factor 1.223
1993 Impact Factor 1.241
1992 Impact Factor 1.559

Impact factor over time

Impact factor

Additional details

5-year impact 2.36
Cited half-life 7.70
Immediacy index 0.53
Eigenfactor 0.01
Article influence 0.75
Website Immunology Letters website
Other titles Immunology letters
ISSN 0165-2478
OCLC 5434613
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details


  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Authors pre-print on any website, including arXiv and RePEC
    • Author's post-print on author's personal website immediately
    • Author's post-print on open access repository after an embargo period of between 12 months and 48 months
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months
    • Author's post-print may be used to update arXiv and RepEC
    • Publisher's version/PDF cannot be used
    • Must link to publisher version with DOI
    • Author's post-print must be released with a Creative Commons Attribution Non-Commercial No Derivatives License
    • Publisher last reviewed on 03/06/2015
  • Classification

Publications in this journal

  • Immunology Letters 11/2015; DOI:10.1016/j.imlet.2015.11.010

  • Immunology Letters 11/2015; S0165-2478(15).
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    ABSTRACT: The bacterial enzyme EndoS specifically cleaves glycans bound to immunoglobulin G (IgG) molecules. Because this deglycosylation procedure leads to a diminished immune response, this enzyme has potential applications as a therapeutic for autoimmune disorders. Although the diminished immune response is attributed to a structural change in the Fc region of IgG antibodies, the specific nature of this structural change is not known due to the variety of results obtained by different experimental approaches. In order to better understand how EndoS deglycosylation impacts the structure of the Fc region of IgG antibodies, we have conducted single molecule Förster resonance energy transfer (FRET) studies of dye-labeled, freely diffusing antibodies. A comparison of the FRET efficiency histograms obtained for glycosylated and EndoS deglycosylated antibodies indicates that the Fc region can take on a wider variety of structures upon deglycosylation. This is demonstrated by the presence of additional peaks in the FRET efficiency histogram for the deglycosylated case.
    Immunology Letters 09/2015; 167(1):29-33. DOI:10.1016/j.imlet.2015.06.011
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    Immunology Letters 04/2015; 165(2). DOI:10.1016/j.imlet.2015.03.012

  • Immunology Letters 04/2015; 164(1):40-43.
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    ABSTRACT: Interleukin-6 (IL-6), a central proinflammatory cytokine, may be involved in the host response to cancer. We therefore aimed to evaluate the association of the IL-6 gene polymorphisms at positions -174 and -572 with predisposition to renal cancer. We conducted a hospital-based case-control study. A total of 432 subjects, including 216 pathologically-proven renal cancer cases and 216 age- and gender-matched healthy controls, were recruited in this study. Polymorphism for the IL-6 gene was genotyped by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Patients with renal cancer had a significantly higher frequency of IL-6 -174 CC genotype [odds ratio (OR)=2.08, 95% confidence interval (CI)=1.05, 4.13; P=0.04] than healthy controls. When stratifying by the grade, patients with higher grade (grade 3 or 4) renal cancer had a significantly higher frequency of IL-6 -174 CC genotype (OR=2.33, 95% CI=1.04, 5.23; P=0.04). This study is, to our knowledge, the first to examine prospectively an increased risk role of IL-6 -174CC genotype in renal cancer susceptibility. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 03/2015; 164(2). DOI:10.1016/j.imlet.2015.03.001
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    ABSTRACT: Therapeutic cancer vaccines are an immunotherapy that amplify or induce an active immune response against tumors. Notably, limitations in the methodology for existing anti-cancer drugs may subsist while applying them to cancer vaccine therapy. A retrospective analysis was performed using information obtained from, PubMed, and published articles. Our research evaluated the optimal methodologies for therapeutic cancer vaccines based on (1) patient populations, (2) immune monitoring, (3) tumor response evaluation, and (4) supplementary therapies. Failure to optimize these methodologies at an early phase may impact development at later stages; thus, we have proposed some points to be considered during the early phase. Moreover, we compared our proposal with the guidance for industry issued by the US Food and Drug Administration in October 2011 entitled "Clinical Considerations for Therapeutic Cancer Vaccines". Consequently, while our research was aligned with the guidance, we hope it provides further insights in order to predict the risks and benefits and facilitate decisions for a new technology. We identified the following points for consideration: (1) include in the selection criteria the immunological stage with a prognostic value, which is as important as the tumor stage; (2) select immunological assays such as phenotype analysis of lymphocytes, based on their features and standardize assay methods; (3) utilize optimal response criteria for immunotherapy in therapeutic cancer vaccine trials; and (4) consider supplementary therapies, including immune checkpoint inhibitors, for future therapeutic cancer vaccines. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 03/2015; 164(2). DOI:10.1016/j.imlet.2015.02.010
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    ABSTRACT: The role of complement in the regulation of T cell immunity has been highlighted recently by several groups. We were prompted to reinvestigate the role of complement receptor type 1 (CR1, CD35) in human T cells based on our earlier data showing that activated human T cells produce C3 (Torok et al. (2012) [48]) and also by results demonstrating that engagement of Membrane Cofactor Protein (MCP, CD46) induces a switch of anti-CD3-activated helper T cells into regulatory T cells (Kemper et al. (2003) [17]). We demonstrate here that co-ligation of CD46 and CD35, the two C3b-binding structures present on activated CD4+ human T cells significantly enhances CD25 expression, elevates granzyme B production and synergistically augments cell proliferation. The role of CR1 in the development of the Treg phenotype was further confirmed by demonstrating that its engagement enhances IL-10 production and reduces IFNγ release by the activated CD4+ T cells in the presence of excess IL-2. The functional in vivo relevance of our findings was highlighted by the immunohistochemical staining of tonsils, revealing the presence of CD4/CD35 double positive lymphocytes mainly in the inter-follicular regions where direct contact between CD4+ T cells and B lymphocytes occurs. Regarding the in vivo relevance of the complement-dependent generation of regulatory T cells in secondary lymphoid organs we propose a scenario shown in the figure. The depicted process involves the sequential binding of locally produced C3 fragments to CD46 and CD35 expressed on activated T cells, which - in the presence of excess IL-2 - leads to the development of Treg cells. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 03/2015; 164(2). DOI:10.1016/j.imlet.2015.02.009
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    ABSTRACT: Immunogenic cell death (ICD) is a new concept appeared in recent years. Despite growing interests of research on ICD, the circumstances that trigger immune responses against dying tumor cells remain largely unknown. It was demonstrated that recombinant Clostridium difficile toxin B (rTcdB) can induce ICD in intoxicated cells, but its mechanism remains unclear. This work aim at exploring whether reactive oxygen species (ROS) involved in rTcdB induced ICD using the chemical agent N-acetyl cysteine (NAC), Diphenylene Iodonium (DPI) and Antimycin A (Anti.A). The results suggested that ROS involved in rTcdB induced apoptosis and autophagy. DPI and Anti.A successfully inhibited the antitumor immune effect induced by rTcdB. As ICD is determined by a variety of factors, rTcdB is a potential tool for further exploring the circumstances that trigger ICD, which may offer us a good choice for designing the new chemotherapeutic drugs with immunogenic properties. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 02/2015; 164(2). DOI:10.1016/j.imlet.2015.02.007
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    ABSTRACT: Gerald M. Edelman began working to the structure of antibodies when joined as graduate student the laboratory of Henry Kunkel in 1958 at the "Rockefeller University" in New York, obtaining his doctorate in 1960. Edelman's focus on the structure of antibodies led to the 1972 Nobel Prize in Physiology or Medicine along with Rodney R. Porter. Edelman and Porter decided to approach the problem of antibodies structure by splitting. In 1959, Porter published a report in which he used the enzyme papain to cleave the antibody molecule into three pieces of about 50,000Da, corresponding to the two Fab (antigen-binding) and constant Fc (crystallizable) fragments. In the same year, Edelman showed that reduction of the disulfide bonds of antibodies in the presence of denaturizing agents led to dissociation of the molecule into smaller pieces, now known to be the light (L) and heavy (H) chains. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 02/2015; 164(2). DOI:10.1016/j.imlet.2015.02.005
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    ABSTRACT: Interferon regulatory factors (IRFs) are named for their ability to bind to and regulate interferon genes when an organism becomes infected with a virus. Numerous studies have revealed the versatile and critical functions of IRFs. In this study, an IRF gene from Lampetra japonica was identified and analyzed using bioinformatic methods. The L. japonica IRF (Lj-IRF) shares high sequence homology with other vertebrate IRFs but low sequence homology with an ascidian IRF-like protein. We also used recombinant Lj-IRF protein (rLj-IRF) to immunize New Zealand rabbits to prepare specific anti-rLj-IRF polyclonal antibodies. Enzyme-linked immunosorbent assays (ELISAs) and Western blotting assays were performed to detect the valence and specificity of the antibody. FACS analysis revealed that the Lj-IRF protein was expressed in approximately 21.14% of leukocytes and 9.60% of supraneural body cells in L. japonica, with immunofluorescence staining indicating a cytoplasmic location. The immunohistochemistry results demonstrated that IRF is distributed in the epithelial cells of the heart, supraneural body, kidneys and gills but is not detectable in intestinals or oral gland tissues. However, the expression of IRF was upregulated in lamprey intestinal tissues upon stimulation with the rLj-HMGB1 protein. Lj-IRF gene expression levels were higher in the rLj-HMGB1-stimulated group than the control group, and the expression level of Lj-IRF was significantly increased in the intestines as determined by quantitative real-time PCR. These results provide a foundation for studying the origin and evolution of the innate immune system in lampreys. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 02/2015; 164(2). DOI:10.1016/j.imlet.2015.02.006
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    Immunology Letters 02/2015; 165(1). DOI:10.1016/j.imlet.2015.02.003
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    ABSTRACT: Chlamydia trachomatis is the etiological agent of the most commonly reported bacterial sexual transmitted infection (STI) in North America and Europe. The control of Chlamydia infection is hindered by the asymptomatic nature of initial infection but the consequence of untreated infection seriously threatens the reproductive health of young women. Unfortunately, there is no licensed vaccine for Chlamydia vaccine, in part due to our incomplete understanding of the immune response to Chlamydia urogenital infection. It has been well established that T cell-mediated immunity plays a dominant role in protective immunity against Chlamydia and thus the importance of B cells is somewhat underappreciated. Here, we summarize recent progress on understanding the role of B cells during Chlamydia genital tract infections and discuss how B cells and humoral immunity make an effective contribution to host defense against important intracellular pathogens, including Chlamydia. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 02/2015; 164(2). DOI:10.1016/j.imlet.2015.02.004
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    ABSTRACT: Jawless vertebrates utilize a form of adaptive immunity that is functionally based on molecular effectors that are completely different from those of vertebrates. This observation raises an intriguing question: Why did vertebrates, representing only 5% of all animals, twice evolve a system as complex as adaptive immunity? Theories aimed at identifying a selective pressure that would 'drive' the development of an adaptive immune system (AIS) fail to explain why invertebrates would not similarly develop an AIS. We argue that an AIS can only be implemented in a certain physiological context, i.e., that an AIS represents an unevolvable trait for invertebrates. The immune system is functionally integrated with other systems; therefore a preexisting physiological innovation unique to vertebrates may have acted as the prerequisite infrastructure that allowed the development of an AIS. We propose that future efforts should be directed towards identifying the evolutionary release that allowed the development of an adaptive immune system in vertebrates. In particular, the advent of specialized adipocytes might have expanded the metabolic scope of vertebrates, allowing the opportunistic incorporation of an AIS. However, physiological innovations, unique to (or more developed in) vertebrates, supports the implementation of an AIS. Thus, understanding the interaction between systems (e.g. neural-immune-adipose connection) may illuminate our understanding regarding the perplexing immunological dimorphism within the animal kingdom. Copyright © 2015. Published by Elsevier B.V.
    Immunology Letters 02/2015; 164(2). DOI:10.1016/j.imlet.2015.02.002
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    ABSTRACT: The human Heat Shock Proteins (HSP70) family plays a key role in up-regulating stress responses. Some studies reported possible associations of single nucleotide polymorphisms in the HSP70 genes with some autoimmune diseases. However, whether HSP70 polymorphisms represent a risk factor for pemphigus foliaceus (PF) is still unkown. We analyzed by PCR-RFLP polymorphisms of HSP70 genes HSA1A, HSPA1B and HSPA1L in 80 Tunisian patients with PF, 160 matched healthy controls and 147 related healthy subjects. There were significant differences between PF patients and controls in the allelic (pc= 5.91 10(-12), pc=1.14 10(-5) and pc=0.0089; respectively) and homozygous genotypic frequencies of HSPA1L>T, HSPA1A>C and HSPA1B>G (p= 2.61710(-12), p= 1.017 10(-5) and p=0.0058; respectively). Haplotype analysis showed significant differences between PF patients and controls: the CCA, CGA, CCG and CGG haplotypes were significantly over-represented in controls whereas the TCG haplotype was significantly over-represented in patients. However, the significant LD found between the HSP70 and the HLA class II susceptibility alleles together with the multivariant regression analysis data between the two loci could argue against a direct role of the HSP70 polymorphism in the occurrence of PF. Copyright © 2015 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.
    Immunology Letters 02/2015; 164(2). DOI:10.1016/j.imlet.2015.01.006