European Journal of Immunology (Eur J Immunol)

Publisher: European Federation of Immunological Societies, Wiley-VCH Verlag

Journal description

The European Journal of Immunology is an international journal focusing on the various aspects of immunological research. One of the world's leading journals of immunology it reports on the latest breakthroughs in the area. The European Journal of Immunology is a well-respected high-impact publication with the best Executive Committee in the field. Top authors have submitted their best papers to the journal for many years therefore building a high quality immunology journal. An ever-increasing amount of papers is being published from top authors from all over the world. The European Journal of Immunology is committed to publishing excellence with a focus on originality topicality and speed of publication. Well balanced coverage of immunology! The European Journal of Immunology provides a monthly forum for top-quality papers on the various aspects of immunological research. Original papers and short communications report the progress being made in the following fields of immunology: immunobiology experimental/human immunology molecular immunology immunopathology immunogenetics clinical immunology The Executive Committee and the international Editorial Board ensure the publication of high quality papers and an international and broad subject coverage. Kurztext Diese Zeitschrift zählt zur Weltspitze der wissenschaftlichen Immunologie-Journale. In ihr erscheinen Originalbeiträge und Kurzmitteilungen aus einem außerordentlich weiten Themengebiet. Hierzu gehören Aspekte der molekularen Immunologie der Immunogenetik der Cytokine der Immunochemie sowie der zellulären und klinischen Immunologie. Es werden außerdem Beiträge zu neuen Entwicklungen experimenteller Methoden und Techniken veröffentlicht. Society Affiliation European Federation of Immunological Societies (EFIS) Readers Immunologists biochemists molecular biologists cell biologists

Current impact factor: 4.03

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 4.034
2013 Impact Factor 4.518
2012 Impact Factor 4.97
2011 Impact Factor 5.103
2010 Impact Factor 4.942
2009 Impact Factor 5.179
2008 Impact Factor 4.865
2007 Impact Factor 4.662
2006 Impact Factor 4.772
2005 Impact Factor 4.876
2004 Impact Factor 5.005
2003 Impact Factor 4.536
2002 Impact Factor 4.832
2001 Impact Factor 4.99
2000 Impact Factor 5.24
1999 Impact Factor 5.635
1998 Impact Factor 5.438
1997 Impact Factor 5.256
1996 Impact Factor 5.701
1995 Impact Factor 6.015
1994 Impact Factor 5.664
1993 Impact Factor 5.577
1992 Impact Factor 4.934

Impact factor over time

Impact factor
Year

Additional details

5-year impact 4.28
Cited half-life 8.50
Immediacy index 0.98
Eigenfactor 0.04
Article influence 1.69
Website European Journal of Immunology website
Other titles European journal of immunology (Online), European Journal of Immunology, EJI
ISSN 1521-4141
OCLC 41614778
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Wiley-VCH Verlag

  • Pre-print
    • Author cannot archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • Upon funder agreement with publisher
  • Conditions
    • Pre-print may be deposited on personal intranet or institutional intranet repository, but not on a public repository
    • Pre-print must not updates with future versions
    • Published source must be acknowledged with set phrases (See policy)
    • Must link to publisher's site: http://www.interscience.wiley.com/
    • Publisher's version/PDF cannot be used
    • Some journal exceptions-check individual homepages
  • Classification
    white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: In addition to MHC restriction and its structural correlate, the recognition of an MHC-peptide complex by the T-cell antigen receptor (TCR), T-cell reactivity is constrained by positive and negative selection in the thymus. While mouse genetic studies have provided compelling evidence for both processes, the actual impact of selection on the mature T-cell repertoire has remained difficult to assess, in particular because it has so far not been possible to follow the intrathymic differentiation of antigen-specific T cells carrying endogenous TCR specificities. In this issue of the European Journal of Immunology, Hesnard et al. [Eur. J. Immunol. 2016. 46: XXXX-XXXX] report the detection of human antigen-specific immature thymocytes, thereby opening the way to addressing these questions. Here we discuss the implications of this technological advance. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: Neutrophils are an abundant cell type in many chronic inflammatory diseases such as rheumatoid arthritis (RA); however, their contribution to the pathology of RA has not been widely studied. A key cytokine involved in neutrophil development and function is granulocyte-colony stimulating factor (G-CSF). In this study we used the K/BxN serum-transfer arthritis (STA) model, mimicking the effector phase of RA, to investigate the importance of G-CSF in arthritis development and its relation to neutrophils. Here, we show for the first time in this model that G-CSF levels are increased both in the serum and in inflamed paws of arthritic mice and importantly that G-CSF blockade leads to a profound reduction in arthritis severity, as well as reduced numbers of neutrophils in blood. Moreover, CXCL1 and CXCL2 levels in the arthritic joints were also lowered. Our data demonstrate that G-CSF is a pivotal driver of the disease progression in the K/BxN STA model and possibly acts in part by regulating neutrophil numbers in the circulation. Therefore, our findings suggest that G-CSF might be a suitable target in RA, and perhaps in other immune complex-driven pathologies. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: The immune system has the ability to specifically identify and eliminate tumours, but the underlying mechanisms responsible for this phenomenon are not fully understood. A study published in this issue of the European Journal of Immunology now provides new insights into this important issue. Joncker et al. [Eur. J. Immunol. 2016. 46: XXXX-XXXX] show that the timely mobilisation of tumour antigen-bearing dendritic cells from the periphery to the lymph nodes is critical for effective anti-tumour T-cell immunity, and that dendritic cells present tumour antigens much more efficiently when encountered in the skin rather than in the subcutaneous tissues. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: Allergic asthma is a chronic inflammatory disease mediated by Th2 cell immune responses. Currently, immunotherapies based on immune deviation are attractive preventive and therapeutic strategies for asthma. Many studies have shown that intracellular bacterial infections such as mycobacteria and their components can suppress asthmatic reactions by enhancing Th1 responses, while helminth infections and their proteins can inhibit allergic asthma via immune regulation. However, some helminth proteins such as SmP40, the major egg antigen of Schistosoma mansoni, are found as Th1 type antigens. Using a panel of overlapping peptides, we identified T-cell epitopes on SjP40 protein of Schistosoma japonicum, which can induce Th1 cytokine and inhibit the production of Th2 cytokines and airway inflammation in a mouse model of allergic asthma. These results reveal a novel form of immune protective mechanism, which may play an important role in the modulating effect of helminth infection on allergic asthmatic reactions. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: Paired immunoglobulin-like type 2 receptor α (PILRα) is an inhibitory receptor that is mainly expressed on myeloid cells, and negatively regulates neutrophil infiltration during inflammation. However, PILRα role on monocyte has not been described. Under both steady-state and inflammatory conditions, monocytes migrate into tissues and differentiate into macrophages. Macrophages in adipose and liver tissues play important roles in tissue homeostasis and pathogenesis of metabolic diseases. Here, we found that PILRα controls monocyte mobility through regulating integrin signaling and inhibiting CD99-CD99 binding. Moreover, we found that Pilra(-/-) mice developed obesity and hepatomegaly with fibrosis, and the numbers of macrophages in adipose and liver tissues are significantly increased in Pilra(-/-) mice. These data suggest that immune inhibitory receptor, PILRα, plays an important role in the prevention of obesity and liver fibrosis. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: NK cells play a central role in the haploidentical HSC transplantation (HSCT) to cure high-risk leukemias. Other innate lymphoid cells (ILCs) have been proposed to exert a protective role in graft-versus-host disease and could also contribute to anti-microbial defence and to lymphoid tissue remodelling. Thus, we investigated the ILC differentiation potential of HSCs isolated from BM, mobilized peripheral blood (PB), and umbilical cord blood (UCB). BM CD34(+) cells are enriched in lymphoid-committed precursors, while PB CD34(+) cells preferentially contain myeloid precursors. In vitro differentiation experiments revealed that the highest and the lowest CD56(+) CD161(+) ILC recovery was detected in UCB and PB HSC cultures, respectively. Among CD56(+) CD161(+) ILCs, the ratio between NK cells and ILC3s was similar for all HSC analyzed. ILC recovery in PB CD34(+) cultures was lower for G-CSF-mobilized HSCs (good mobilizers) than for G-CSF+plerixafor-mobilized HSC (poor mobilizers). Moreover, G-CSF inhibited in vitro ILC recovery and the degree of inhibition was proportional to the time of exposure to the cytokine. Thus, although all common sources of HSC for transplant differentiate towards ILCs, substantial differences exist among different sources and G-CSF may influence ILC recovery. These data offer new clues for a better understanding of the immune reconstitution after HSCT. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: It has been shown that while commensal bacteria promote Th1, Th17, and Treg cells in lamina propria (LP) in steady-state conditions, they suppress mucosal Th2 cells. However, it is still unclear whether there are specific commensal organisms down-regulating Th2 responses, and the mechanism involved. Here we demonstrate that commensal A4 bacteria, a member of the Lachnospiraceae family, which produce an immunodominant microbiota CBir1 antigen, inhibits LP Th2-cell development. When transferred into the intestines of RAG(-/-) mice, CBir1-specific T cells developed predominately towards Th1 cells and Th17 cells, but to a lesser extent into Th2 cells . The addition of A4 bacterial lysates to CD4(+) T-cell cultures inhibited production of IL-4. A4 bacteria stimulated dendritic cell production of TGF-β, and blockade of TGF-β abrogated A4 bacteria inhibition of Th2-cell development in vitro and in vivo. Collectively, our data show that A4 bacteria inhibit Th2-cell differentiation by inducing dendritic cell production of TGF-β. This article is protected by copyright. All rights reserved.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: The German Society for Immunology (DGfI) and the Australasian Society for Immunology (ASI) hosted the first DGfI-ASI joint workshop from December 3-4, 2015 in Canberra, Australia. A delegation of 15 distinguished German immunologists discussed the workshop topic "immune regulation in infections and immune mediated diseases" with the aim to establish new German-Australasian collaborations, discuss new concepts in the field of immune regulation and build a scientific network to create more utilizable resources for excellent (trans-border) immunological research. The workshop was associated with the 45(th) Annual Scientific Meeting of the ASI held from Nov 29-Dec 3, 2015, opening up even more opportunities for finding new collaboration partners. A return meeting will be linked to the annual DGfI meeting that will take place in 2017 in Erlangen.
    No preview · Article · Feb 2016 · European Journal of Immunology
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    ABSTRACT: The innate immune system represents the first line of defense during infection and is initiated by the detection of conserved microbial products by germline-encoded pattern recognition receptors (PRRs). Sensing through PRRs induces broad transcriptional changes that elicit powerful inflammatory responses. Tight regulation of these processes depends on multiple regulatory checkpoints, including noncoding RNA species such as microRNAs. In addition, long noncoding RNAs (lncRNAs) have recently gained attention as important regulators of gene expression acting through versatile interactions with DNA, RNA, or proteins. As such, these RNAs have a multitude of mechanisms to modulate gene expression. Here, we summarize recent advances in this rapidly moving and evolving field. We highlight the contribution of lncRNAs to both the development and activation of innate immune cells, whether it is in the nucleus, where lncRNAs alter the transcription of target genes through interaction with transcription factors, chromatin modifying complexes or heterogenous ribonucleoprotein complexes, or in the cytosol where they can control the stability of target mRNAs. In addition, we discuss experimental approaches required to comprehensively investigate the function of a candidate noncoding RNA locus, including loss-of-function approaches encompassing genomic deletions, RNA interference, locked nucleic acids and various adaptions of the CRISPR/Cas9 technology. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: Thymic epithelial cells (TECs) provide essential signals for αβT-cell development, and medullary TECs (mTECs) control T-cell tolerance through both negative selection and Foxp3(+) Regulatory T (Treg)-cell development. Although heterogeneity within the mTEC compartment is well studied, the molecular regulators of specific stages of mTEC development are still poorly understood. Given the importance of the RANK-RANKL axis in thymus medulla formation, we have used RANK Venus reporter mice to analyse the ontogeny of RANK(+) TECs during development, and correlated RANK expression with mTEC stem cells defined by SSEA1. In addition, we have investigated how requirements for the key regulators Foxn1 and Relb map to specific stages of mTEC development. Here, we show SSEA-1(+) mTEC stem cells emerge prior to RANK expression and are present in both nude and Relb(-/-) mice, providing direct evidence that mTEC lineage specification occurs independently of Foxn1 and Relb. In contrast, we show that Relb is necessary for the effective production of downstream RANK(+) mTEC progenitors. Collectively, our work defines stage-specific requirements for critical TEC regulators during medulla development, including the timing of Relb dependency, and provides new information on mechanisms controlling mTEC specification. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: While the functional plasticity of memory CD4(+) T cells has been studied extensively, less is known about this property in memory CD8(+) T cells. Here we report the direct measurement of plasticity by paired daughter analysis of effector and memory OT-I CD8(+) T cells primed in vivo with ovalbumin. Naïve, effector and memory OT-I cells were isolated and activated in single-cell culture then, after the first division, their daughter cells were transferred to new cultures with and without IL-4; expression of IFN-γ and IL-4 mRNAs was measured 5 days later in the resultant subclones. Approximately 40% of clonogenic memory CD8(+) T cells were bipotential in this assay, giving rise to an IL-4(-) subclone in the absence of IL-4 and an IL-4(+) subclone in the presence of IL-4. The frequency of bipotential cells was lower among memory cells than naïve cells but markedly higher than among 8-day effectors. Separation based on high or low expression of CD62L, CD122, CD127 or Ly6C did not identify a phenotypic marker of the bipotential cells. Functional plasticity in memory CD8(+) T-cell populations can therefore reflect modulation at the level of a single memory cell and its progeny. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: The mechanism by which the DNA deaminase AID is specifically recruited to repetitive switch region DNA during class switch recombination is still poorly understood. Work over the past decade has revealed a strong link between transcription and RNA polymerase-associated factors in AID recruitment, yet none of these processes satisfactorily explain how AID specificity is effected. Here we review a recent finding wherein AID is guided to switch regions not by a protein factor but by an RNA moiety, and especially one associated with a non-coding RNA that has been long thought of as being inert. This work explains the long-standing requirement of splicing of non-coding transcripts during class switching, and has implications in both B-cell-mediated immunity as well as the underlying pathological syndromes associated with the recombination reaction. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: Neutrophil extracellular traps (NETs) are a combination of DNA fibers and granular proteins, such as neutrophil elastase (NE). NETs are released in the extracellular space in response to different stimuli. Carrageenan is a sulfated polysaccharide extracted from Chondrus crispus, a marine algae, used for decades in research for its potential to induce inflammation in different animal models. In this study, we show for the first time that carrageenan injection can induce NET release in a mouse model of acute peritonitis. Carrageenan induced NET release by viable neutrophils with neutrophil elastase (NE) and myeloperoxidase (MPO) expressed on DNA fibers. Furthermore, although this polysaccharide was able to stimulate reactive oxygen species (ROS) generation by peritoneal neutrophils, NADPH oxidase-derived ROS were dispensable for NET formation by carrageenan. In conclusion, our results show that carrageenan-induced inflammation in the peritoneum of mice can induce NET formation in a ROS-independent manner. These results may add important information to the field of inflammation and potentially lead to novel anti-inflammatory agents targeting the production of NETs. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: CpG oligodeoxynucleotide (ODN) is one of promising nucleic acid-based adjuvants. We recently improved its ability to enhance CD8(+) T-cell responses to co-administered protein antigen without conjugation or emulsion, by forming a nano-particulate complex between CpG ODN (K3) and mushroom derived β-glucan schizophyllan (SPG), namely K3-SPG. Here, we sought to elucidate the cellular immunological mechanisms by which K3-SPG induce such potent CD8(+) T-cell responses to co-administered antigen. By focusing on two DC subsets, plasmacytoid DCs and CD8α(+) DCs, as well as the secreted cytokines, IFN-α and IL-12, we found that K3-SPG strongly activates mouse plasmacytoid DCs to secrete IFN-α and CD8α(+) DCs to secrete IL-12 respectively. Although a single cytokine deficiency had no impact on adjuvant effects, the lack of both type I IFN and IL-12 in mice resulted in a significant reduction of Th1 type immune responses and CD8(+) T-cell responses elicited by protein vaccine model. By sharp contrast, type I IFN, but not IL-12, was required for the production of IFN-γ by human PBMCs as well as antigen-specific CD8(+) T-cell proliferation. Taken together, K3-SPG may overcome the species barrier for CpG ODN to enhance antigen-specific CD8(+) T-cell responses despite the differential role of IL-12 between human and mice. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: Osteoclast Associated Receptor (OSCAR) is an activating receptor expressed by human myeloid cells. Collagen type I (ColI) and collagen type II (ColII) serve as ligands for OSCAR. OSCAR-collagen interaction stimulates RANK-dependent osteoclastogenesis. We have recently reported that OSCAR promotes functional maturation of monocyte-derived dendritic cells (moDCs). OSCAR is up-regulated on monocytes from rheumatoid arthritis (RA) patients with active disease, and these monocytes show an increased pro-osteoclastogenic potential. In the current study, we have addressed a functional role for an OSCAR-collagen interaction on monocytes. We show that OSCAR-ColII signaling promoted the survival of monocytes. Moreover, ColII stimulated the release of pro-inflammatory cytokines by monocytes from healthy donors, which could be completely blocked by an anti-OSCAR monoclonal antibody. Mononuclear cells from the synovial fluid of RA patients plated on ColII secreted TNF-α and IL-8 in an OSCAR-dependent manner. Global RNA profiling showed that components of multiple signaling pathways relevant to RA pathogenesis are regulated at the transcriptional level by OSCAR in monocytes. Thus, OSCAR can play a pro-inflammatory role in monocyte-derived cells and may contribute crucially on multiple levels to RA pathogenesis. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: Fibrostrictures (FS) are a major complication of Crohn's disease (CD). Pathogenesis of FS is not fully understood, but activation of fibroblasts and excessive collagen deposition are crucial in the development of FS. Here we investigated the role of aryl hydrocarbon receptor (AhR) in intestinal fibrosis. AhR RNA and protein expression was evaluated in intestinal fibroblasts of CD patients and controls. CD fibroblasts were stimulated with TGF-β1 or TNF-α in the presence or absence of the AhR activator Ficz, an AhR antagonist CH223191, or a specific AhR-silencing RNA. In CD fibroblasts, TGF-β1 and TNF-α increased Col1A1, Col3A1 and α-SMA transcripts and collagen secretion and this effect was reduced by Ficz and upregulated by CH22319. TGF-β1 or TNF-α-induced activation of p38 and ERK1/2 MAP kinases was decreased by Ficz and increased by CH223191. The inhibitory effect of Ficz on Map kinase activation and collagen induction was abolished by AhR silencing. To assess the role of AhR in vivo, mice with trinitrobenzene-sulfonic-acid(TNBS)-induced colonic fibrosis were given Ficz or CH223191. Mice given either Ficz or CH223191 produced less or more collagen respectively as compared with control mice. Our results indicate that AhR is a negative regulator of pro-fibrotic signals in the gut. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: The induction of a pan-immunosuppressive state is a central feature of persistent viral infections. Over the past decade, multiple pathways have been identified that contribute to immune suppression. Recently, it was revealed that aberrant or sustained type 1 interferon (IFN-I) production or signaling is a central contributor to immune suppression elicited during persistent viral infection. In this issue, Honke et al. [Eur. J. Immunol. 2016. 46: XXX-XXXX] identify that IFN-I signaling promotes an immune suppressive state during persistent lymphocytic choriomeningitis virus (LCMV) infection by inhibiting enforced virus replication in CD169+ macrophages. The authors demonstrate that mice infected with a persistent strain of LCMV have blunted humoral immune responses to a superinfecting vesicular stomatitis virus (VSV) infection. The absence of virus replication in CD169+ macrophages was not due to anti-viral CD8+ T cell-mediated killing of CD169+ macrophages, but required sustained IFN-I responses. In turn, reduction in VSV replication in CD169+ macrophages resulted in a reduction in antigen production, which is necessary for generating optimal humoral responses. This study highlights a novel mechanism by which IFN-I signaling promotes an immune suppressive state during persistent viral infection. This article is protected by copyright. All rights reserved
    No preview · Article · Jan 2016 · European Journal of Immunology
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    ABSTRACT: T-cell development occurs in multipotent progenitors arriving in the thymus, which provides a highly specialized microenvironment. Specification and sequential commitment processes to T cells begin in early thymic progenitors upon receiving thymus-specific environmental cues, resulting in the activation of the genetically programmed transcriptional cascade that includes turning on and off numerous transcription factors in a precise manner. Thus, early thymocyte differentiation has been an excellent model system to study cell differentiation processes. This review summarizes recent advances in our knowledge on thymic T-cell development from newly arrived multipotent T-cell progenitors to fully committed T-cell precursors, from the transcriptional regulation perspective. This article is protected by copyright. All rights reserved.
    No preview · Article · Jan 2016 · European Journal of Immunology