International Immunology (INT IMMUNOL)

Publisher: Oxford University Press (OUP)

Journal description

International Immunology publishes a broad range of experimental and theoretical studies in molecular and cellular immunology conducted in laboratories throughout the world.

Current impact factor: 2.54

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.536
2013 Impact Factor 3.181
2012 Impact Factor 3.135
2011 Impact Factor 3.415
2010 Impact Factor 3.301
2009 Impact Factor 3.403
2008 Impact Factor 3.181
2007 Impact Factor 3.29
2006 Impact Factor 4.015
2005 Impact Factor 3.317
2004 Impact Factor 3.543
2003 Impact Factor 3.69
2002 Impact Factor 3.595
2001 Impact Factor 3.611
2000 Impact Factor 3.13
1999 Impact Factor 2.897
1998 Impact Factor 3.188
1997 Impact Factor 3.548
1996 Impact Factor 4.485
1995 Impact Factor 4.333
1994 Impact Factor 4.185
1993 Impact Factor 3.954
1992 Impact Factor 3.841

Impact factor over time

Impact factor

Additional details

5-year impact 3.08
Cited half-life 9.60
Immediacy index 0.83
Eigenfactor 0.01
Article influence 1.15
Website International Immunology website
Other titles International immunology online., International immunology
ISSN 0953-8178
OCLC 20567176
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Oxford University Press (OUP)

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    • 12 months embargo
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    • Publisher's version/PDF cannot be used
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    • Set phrase to accompany archived copy (see policy)
    • Eligible authors may deposit in OpenDepot
    • The publisher will deposit in PubMed Central on behalf of NIH authors
    • Publisher last contacted on 19/02/2015
    • This policy is an exception to the default policies of 'Oxford University Press (OUP)'
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The adaptive immune response is involved in the development and progression of atherosclerosis and IL-17A(+) cells play a role in this disease. While elevated number of CD4(+) IL-17A(+) (Th17) and IL-17A(+)TCRγδ(+) T cells are found within murine atherosclerotic aortas and human plaques, the mechanisms governing IL-17A(+) T cell migration to atherosclerotic lesions are unclear. The chemokine receptor CXCR6 is expressed on several T cell subsets and plays a pro-atherogenic role in atherosclerosis. Here, we used CXCR6-deficient (Cxcr6(GFP/GFP)) Apolipoprotein E-deficient (Apoe(-/-)) mice to investigate the involvement of CXCR6 in the recruitment IL-17A(+) T cells to atherosclerotic aortas. Flow cytometric analyses revealed reductions in Th17 and IL-17A(+)TCRγδ(+) T cells within aged Cxcr6(GFP/GFP)Apoe(-/-) aortas, in comparison with age matched Cxcr6(GFP/+)Apoe(-/-) aortas. While CXCR6-sufficient IL-17A(+) T cells efficiently migrated towards CXCL16, the migration of CXCR6-deficient IL-17A(+) T cells was abolished in transwell assays. Importantly, the recruitment of Cxcr6(GFP/GFP)Apoe(-/-) IL-17A(+) T cells into the aortas of Apoe(-/-) recipients was markedly reduced in short-term adoptive transfer experiments. Altogether these results demonstrate an important role of CXCR6 in the regulation of pathological Th17 and IL-17A(+)TCRγδ(+) T cell recruitment into atherosclerotic lesions.
    International Immunology 11/2015; DOI:10.1093/intimm/dxv068
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    ABSTRACT: The toll-like receptors (TLRs) are important innate receptors recognizing potentially pathogenic material. However, they also play a significant role in the development of Alzheimer's disease, cancer, autoimmunity and the susceptibility to viral infections. Macrophages are essential for an effective immune response to foreign material and the resolution of inflammation. In these studies we examined the impact of different TLR ligands on macrophage cell function. We demonstrate that stimulation of all TLRs tested increases the phagocytosis of apoptotic cells. TLR7 and TLR9 ligation decreased the levels of the surface co-expression molecules CD86 and MHC-II, which was associated with a concomitant reduction in antigen presentation and proliferation of T cells. This down-regulation in macrophage function was not due to an increase in cell death. In fact, exposure to TLR7 or TLR9 ligands promoted cell viability for up to 9 days, in contrast to TLR3 or TLR4. Additionally, macrophages exposed to TLR7/TLR9 ligands, had a significantly lower ratio of Il-12/Il-10 mRNA expression compared to those treated with the TLR4 ligand, LPS. Taken together these data demonstrate that TLR7/TLR9 ligands push the macrophage into a phagocytic, long-lived cell, with a decreased capacity of antigen presentation and reminiscent of the M2 polarized state.
    International Immunology 11/2015; DOI:10.1093/intimm/dxv066
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    ABSTRACT: Leptin, one of the typical adipokines, is reported to promote Th17 cell responses and to enhance production of proinflammatory cytokines. To clarify the role of leptin in the regulation of the IL-23/IL-17 axis and the development of kidney disease, we used a murine model of nephrotoxic serum (NTS) nephritis (NTN). Sheep NTS was administered in wild-type C57BL/6J mice and food-restricted, leptin-deficient C57BL/6J-ob/ob (FR-ob/ob) mice after preimmunization with sheep IgG. The profile of mRNA expression relevant to T helper lymphocytes in the kidneys was analyzed by quantitative real-time PCR (qRT-PCR). Cultured murine glomerular podocytes and peritoneal exudate macrophages (PEMs) were used to investigate the direct effect of leptin on IL-23 or MCP-1 production by qRT-PCR. Kidney injury and macrophage infiltration was significantly attenuated in FR-ob/ob mice 7 days after NTS injection. Th-17-dependent secondary immune response against deposited NTS in the glomeruli was totally impaired in FR-ob/ob mice due to deteriorated IL-17 and proinflammatory cytokine production including IL-23 and MCP-1 in the kidney. IL-23 was produced in glomerular podocytes in NTN mice and cultured murine glomerular podocytes produced IL-23 under leptin stimulation. MCP-1 production in PEMs was also promoted by leptin. Induction of MCP-1 expression was observed in PEMs regardless of Ob-Rb, and leptin signal was transduced without STAT3 phosphorylation in PEMs. Leptin deficiency down-regulates IL-23 production and Th17 responses in the NTN kidney, followed by impaired secondary immune responses against NTS, which is accompanied by decreased MCP-1 production and macrophage infiltration in the NTN kidney.
    International Immunology 11/2015; DOI:10.1093/intimm/dxv067

  • International Immunology 11/2015; 27(10). DOI:10.1093/intimm/dxv047
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    ABSTRACT: Group 2 innate lymphoid cells (ILC2) are now recognized as an important innate source of type-2 effector cytokines. Although initially associated with mucosal tissues, it is clear that ILC2 are present in diverse anatomical locations. The function of ILC2 at these sites is equally varied, and although ILC2 represent a relatively minor population, they are fundamentally important regulators of innate and adaptive immune processes. As such, there is much interest to understand the role of ILC2 in diseases with a type-2 inflammatory component. This review explores the known roles of ILC2 in disease, and the diseases that show associations or other strong evidence for the involvement of ILC2. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 08/2015; DOI:10.1093/intimm/dxv050
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    ABSTRACT: CD20(+)CD27(+)CD43(+) B (CD43(+) B) cells have been newly defined among peripheral blood mononuclear cells (PBMCs) and proposed to be human B1 cells. However, it is controversial as to whether they are orthologs of murine B1 cells and how they are related to other B cell populations, particularly CD20(+)CD27(+)CD43(-) memory B cells and CD20(low)CD27(high)CD43(high) plasmablasts. Our objective is to identify phenotypically the position of CD43(+) B cells among peripheral B-lineage cell compartments in healthy donors, with reference to B cell subsets from patients with systemic lupus erythematosus (SLE). We found that CD43(+) B cells among PBMCs from healthy subjects were indistinguishable phenotypically from memory B cells in terms of surface markers, and spontaneous in vitro Ig and IL-10 secretion capability, but quite different from plasmablasts. However, a moderate correlation was found in the frequency of CD43(+) B cells with that of plasmablasts in healthy donors but not in SLE patients. An in vitro differentiation experiment indicated that CD43(+) B cells give rise to plasmablasts more efficiently than do memory B cells, suggesting that they are more closely related to plasmablasts developmentally than are memory B cells, which is also supported by quantitative PCR analysis of mRNA expression of B-cell and plasma-cell signature genes. Thus, we conclude that, in healthy individuals, CD43(+) B cells are closely related not only to memory B cells phenotypically but also to plasmablasts developmentally, although the developmental origin of CD43(+) B cells is not necessarily the same as that of plasmablasts. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 03/2015; 27(7). DOI:10.1093/intimm/dxv009
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    ABSTRACT: Dimethyl fumarate (DMF) is a modifier of the nuclear factor (erythroid-derived 2)-2 (Nrf2) - kelch-like ECH-associated protein 1 (Keap1) pathway. DMF-treatment in the effector phase significantly suppressed the development of Theiler's murine encephalomyelitis virus - induced demyelinating disease (TMEV-IDD) both clinically and histologically. DMF treatment leads to enhance Nrf2 antioxidant response in TMEV-IDD mice. DMF treatment in effector phase significantly suppressed the level of IL-17A mRNA. DMF is known to inhibit differentiation of Th17 via suppressing NF-κB. Taken together, our data suggest that DMF treatment in effector phase may suppress TMEV-IDD not only via enhancing antioxidant response but also via suppressing IL-17A. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 02/2015; 27(7). DOI:10.1093/intimm/dxv006
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    ABSTRACT: Inflammatory bowel disease is thought to be a complex multifactorial disease, in which increased inflammatory response plays an important role. Paired immunoglobulin-like type 2 receptor α (PILRα), well conserved in almost all mammals, is an inhibitory receptor containing immunoreceptor tyrosine-based inhibitory motif (ITIM) in the cytoplasmic domain. PILRα is mainly expressed on myeloid cells and plays an important role in the regulation of inflammation. In the present study, we investigated the function of PILRα in inflammatory bowel diseases using PILRα-deficient mice. When mice were orally administered dextran sodium sulfate (DSS), colonic mucosal injury and inflammation were significantly exacerbated in DSS-treated PILRα-deficient mice compared with wild-type (WT) mice. Flow cytometric analysis revealed that neutrophils and macrophages cell numbers were higher in the colons of DSS-treated PILRα-deficient mice than in those of WT mice. Blockade of CXCR2 expressed on neutrophils using a CXCR2 inhibitor decreased the severity of colitis observed in PILRα-deficient mice. These results suggest that PILRα negatively regulates inflammatory colitis by regulating the infiltration of inflammatory cells such as neutrophils and macrophages. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 02/2015; 27(6). DOI:10.1093/intimm/dxv004
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    ABSTRACT: NKT follicular helper cells (NKTfh) are a recently discovered functional sub-set of CD1d-restricted NKT cells. Given the potential for NKTfh cells to promote specific Ab responses and germinal center reactions, there is much interest in determining the conditions under which NKTfh cells proliferate and/or differentiate in vivo and in vitro. We confirm that NKTfh cells expressing the canonical semi-invariant Vα14 TCR were CXCR5(+)/ICOS(+)/PD-1(+)/Bcl6(+) and increased in number following administration of the CD1d-binding glycolipid α-galactosylceramide (α-GC) to C57Bl/6 mice. We show that the α-GC-stimulated increase in NKTfh cells was CD1d-dependent since the effect was diminished by reduced CD1d expression. In vivo and in vitro treatment with α-GC, singly or in combination with IL-2, showed that NKTfh cells increased in number to a greater extent than total NKT cells, but proliferation was near-identical in both populations. Acquisition of the NKTfh phenotype from an adoptively-transferred PD-1-depleted cell population was also evident, showing that peripheral NKT cells differentiated into NKTfh cells. Therefore, the α-GC-stimulated, CD1d-dependent increase in peripheral NKTfh cells is a result of cellular proliferation and differentiation. These findings advance our understanding of the immune response following immunization with CD1d-binding glycolipids. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 02/2015; 27(5). DOI:10.1093/intimm/dxv007
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    ABSTRACT: The aim of this study was to evaluate the association between the HLA-G 14bp dele-tion/insertion (Del/Ins) polymorphism and soluble (s) HLA-G production in patients with Crohn's disease (CD). We analyzed also the sHLA-G molecules by ELISA and Western Blot in plasma samples. Among unselected patients, the 14bp Del/Ins polymorphism was not sig-nificantly associated with increased Crohn's disease risk neither for alleles (p=0.371) nor for genotypes (p=0.625). However, a significant association was reported between the 14bp Del/Ins polymorphism and CD, in particular in young-onset CD patients for alleles (p=0.020, OR= 2.438, 95%CI: 1.13-5.25) but not with adult-onset CD patients. A significant associa-tion was reported concerning the genotype Ins/Ins for young-onset CD patients (p=0.029, OR=3.257, 95%CI:1.08-9.77). We observed also a significant increase in sHLA-G dosed by ELISA in CD patients compared to controls (p=0.002). The 14bp Del/Del and 14bp Del/Ins genotypes are the high HLA-G producers. Among sHLA-G(positive) patients, a 43% of subjects present dimers of HLA-G. The presence of dimers seems to be related to the advanced stages of the disease. The 14bp Del/Ins polymorphism is associated with an increased risk of CD particularly in young-onset CD patients and controls sHLA-G plasma levels. Dimers of sHLA-G are frequent in advanced disease stages. The above findings indicate that the genetic 14bp Del/Ins polymorphism in the exon 8 of HLA-G gene is associated with the risk of CD, and suggest a role for sHLA-G as prognostic marker for progressive disease. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 01/2015; 27(6). DOI:10.1093/intimm/dxv002
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    ABSTRACT: The anaemia of chronic disease results from inflammation-mediated up-regulation of the iron-regulatory hormone hepcidin, with the consequent sequestration of iron limiting its availability for erythropoiesis. The inflammatory cytokine interleukin-6 (IL6), a regulator of hepcidin, has been implicated in this process. Recent in vivo and in vitro studies indicate that interleukin-22 (IL-22) is also able to stimulate hepcidin expression. We aimed to determine if IL-22 had a role in causing the hypoferremia associated with the inflammatory response. Wild-type and Il22 knockout mice were subjected to an acute inflammatory stimulus via administration of lipopolysaccharide (LPS) and the response of hepcidin and iron homeostasis analysed. In the absence of IL-22 there was a response of hepcidin, resulting in a reduction in serum iron levels. However, the hypoferremic response to LPS was slightly blunted in mice lacking IL-22, suggesting that, during LPS-mediated inflammation, IL-22 may play a minor role in mediating the hypoferremic response. These results may have implications for the treatment and management of the anaemia of chronic disease. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 01/2015; 27(6). DOI:10.1093/intimm/dxu144
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    ABSTRACT: Drak2 is a promising therapeutic target to treat organ-specific autoimmune diseases such as type 1 diabetes and multiple sclerosis without causing generalized immune suppression. Inhibition of Drak2 may also prevent graft rejection following organ in various tumor cell lines, which would challenge the prospect of targeting Drak2 for therapeutic treatment. Thus, we examined the susceptibility of Drak2(-/-) mice in several tumor models. We show that Drak2 is not required to prevent tumor formation in a variety of settings. Therefore, Drak2 does not function as an essential tumor suppressor in in vivo tumor models. These data further validate Drak2 as a viable therapeutic target to treat autoimmune disease and graft rejection. Importantly, these data also indicate that while Drak2 may induce apoptosis when overexpressed in cell lines, it is not an essential tumor suppressor. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 01/2015; 27(3). DOI:10.1093/intimm/dxu146
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    International Immunology 01/2015; 27(1):1-2. DOI:10.1093/intimm/dxu106
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    ABSTRACT: A canonical pre-TCR/TCR signaling pathway critical for thymic T cell development involves sequential phosphorylation and signaling through Lck, Zap70, Lat, and Slp76. However, we and others have previously reported that genomic deletion of c-Cbl (Cbl) partially or completely reverses the defects in thymic development in mice deficient in Zap70, Slp76, Lat, or Vav1, indicating the presence of alternative pathways normally suppressed by Cbl. To further elucidate pre-TCR/TCR signaling pathways involved in thymic development, we characterized the effect of Cbl inactivation on developmental and signaling defects in mice deficient in proximal signaling molecules Lck and Zap70. Inactivation of Cbl partially reversed defective T cell development in Zap70(-/-) mice and reversed defects in phosphorylation of Erk, Plc-γ1, Vav1, and Akt, in TCR-stimulated Cbl(-/-)Zap70(-/-) thymocytes. Recent reports identified an essential role of Lck in associating with CD4 and CD8 coreceptors and mediating the requirement for MHC restriction in TCR recognition. Since TCR recognition has been shown to be MHC-restricted in Cbl(-/-) mice, it was of interest to determine whether the requirement for Lck remained unmodified by Cbl deletion, Indeed, in contrast to the effect of Cbl inactivation in partially or fully bypassing requirements for other TCR signaling components, inactivation of Cbl did not reverse either defective T cell developmental or defective phosphorylation of TCR signaling molecules in Lck(-/-) mice. Thus, Lck, which plays a unique role in enforcing MHC restriction, is essential for thymic development in presence or absence of Cbl, ensuring MHC restriction of T cells derived from either pathway. Published by Oxford University Press on behalf of The Japanese Society for Immunology 2014.
    International Immunology 12/2014; 27(5). DOI:10.1093/intimm/dxu105
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    ABSTRACT: The respiratory syncytial virus (RSV) is responsible for as many as 199,000 annual deaths worldwide. Currently there is no standard treatment for RSV disease, and no vaccine. Sendai virus is an attractive pediatric vaccine candidate because it elicits robust and long-lasting virus-specific B cell and T cell activities in systemic and mucosal tissues. The virus serves as a gene delivery system as well as a Jennerian vaccine against its close cousin, human parainfluenza virus type 1. Here is described the testing of a recombinant SeV (SeVRSV-Fs) that expresses an unconstrained, secreted RSV-F protein as a vaccine against RSV in cotton rats. After a single intranasal immunization of cotton rats with SeVRSV-Fs, RSV-specific binding and neutralizing antibodies were generated. These antibodies exhibited cross-reactivity with both RSV A and B isolates. RSV-F-specific interferon-γ-producing T cells were also activated. The SeVRSV-Fs vaccine conferred complete protection against RSV challenge without enhanced immunopathology. In total, results showed that an SeV recombinant that expresses RSV F in an unconstrained, soluble form can induce humoral and cellular immunity that protects against infection with RSV. © The Japanese Society for Immunology. 2014. All rights reserved. For permissions, please e-mail:
    International Immunology 12/2014; 27(5). DOI:10.1093/intimm/dxu107