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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    • 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
    ​ yellow

Publications in this journal

  • 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: Active vitamin D (1,25D3) blocks the development of experimental autoimmune diseases. However, the molecular and immunobiological mechanisms underlying 1,25D3's anti-inflammatory properties are not fully understood. We employed a murine model of experimental autoimmune encephalomyelitis (EAE) in order to determine the role of NKT cells in 1,25D3-mediated protection from EAE. WT mice or mice lacking all NKT cells (CD1d(-/-)) or invariant NKT cells (Jα18(-/-)) were fed control or 1,25D3 supplemented diets. All mice fed control diet developed severe EAE. 1,25D3 treatment of WT mice protected them from developing EAE. CD1d(-/-) and Jα18(-/-) mice treated with 1,25D3 were not protected to the same extent as WT mice. MOG-specific IL-17 and IFN-γ production was significantly reduced in 1,25D3 WT mice compared to WT but was not decreased in 1,25D3 CD1d(-/-) mice compared to CD1d(-/-) mice. IL-4(-/-) mice were utilized to determine how IL-4 deficiency affects susceptibility to EAE. IL-4(-/-) mice were not protected from developing EAE by α-GalCer or 1,25D3 treatment. Furthermore, 1,25D3 treatment of splenocytes in vitro decreased α-GalCer-induced IL-17 and increased IL-4, IL-5 and IL-10 production. 1,25D3 alters the cytokine profile of iNKT cells in vitro. These studies demonstrate that NKT cells are important mediators of 1,25D3-induced protection from EAE in mice and NKT cell-derived IL-4 may be an important factor in providing this protection. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail:
    International Immunology 01/2015; 27(5). DOI:10.1093/intimm/dxu147
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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
  • 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
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    ABSTRACT: If Bcl11b activity is compromised, CD4(+)CD8(+) double-positive (DP) thymocytes produce a greatly increased fraction of innate CD8(+) single-positive (SP) cells highly producing IFN-γ, which are also increased in mice deficient of genes such as Itk, Id3 and NF-κB1 that affect TCR signaling. Of interest, the increase in the former two is due to the bystander effect of IL-4 that is secreted by PLZF-expressing NKT and γδT cells whereas the increase in the latter is cell intrinsic. Bcl11b zinc-finger proteins play key roles in T cell development and T cell-mediated immune response likely through TCR signaling. We examined thymocytes at and after the DP stage in Bcl11b(F/S826G) CD4cre, Bcl11b(F/+) CD4cre, and Bcl11b(+/S826G) mice, carrying the allele that substituted serine for glycine at the position of 826. Here we show that Bcl11b impairment leads to an increase in the population of TCRαβ(high)CD44(high)CD122(high) innate CD8SP thymocytes, together with two different developmental abnormalities: impaired positive and negative selection accompanying a reduction in the number of CD8SP cells, and developmental arrest of NKT cells at multiple steps. The innate CD8SP thymocytes express Eomes and secrete IFN-γ after the stimulation with PMA and ionomycin, and in this case their increase is not due to a bystander effect of IL-4 but cell intrinsic. Those results indicate that Bcl11b regulates development of different thymocyte subsets at multiple stages and prevents the excess of innate CD8SP thymocytes. © The Japanese Society for Immunology. 2014. All rights reserved. For permissions, please e-mail:
    International Immunology 11/2014; 27(4). DOI:10.1093/intimm/dxu104
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    ABSTRACT: Endometriosis is a significant debilitating gynecological problem affecting women of reproductive age group and post-menopause. Recent reports prompt at the role of endometriotic Mesenchymal Stem Cells (ectopic MSCs) in pathogenesis of endometriosis. To investigate the plausible mechanisms leading to the pathogenic behavior of ectopic MSCs, we compared the immunomodulatory properties of eutopic and ectopic (healthy) MSCs. We analyzed MSC phenotypes, differential gene expression for an array of pattern recognition receptors (PRRs) and pro-inflammatory cytokine release along with markers of migration and angiogenesis among eutopic and ectopic MSCs. Further, alterations in immunosuppressive functions of eutopic and ectopic MSCs were examined by co-culturing them with mitogen-activated allogenic PBMCs. Transcripts of PRRs such as all Toll-like Receptors (TLR 1-10), except TLR8, collectins (CL-L1, CL-P1, CL-K1), NOD-1 and 2 receptors, secreted pro-inflammatory cytokines like IL-6, IFNγ, VEGF, EGF, MCP-1 were significantly upregulated in ectopic MSCs. The anti-inflammatory cytokine TGFβ showed significant downregulation, while IL-10 showed a significant increase in ectopic MSCs. Further, ectopic MSCs showed upregulated expression for markers of migration and angiogenesis such as MMP - 2, 3, 9 and VEGF respectively. We report here that proliferation of PBMCs was less inhibited upon co-culture with ectopic MSCs compared with eutopic MSCs. The findings suggest that ectopic MSCs with increased levels of TLRs, collectins, pro-inflammatory cytokines and markers of migration and angiogenesis, exhibit a distinct immune-phenotype compared to eutopic MSCs. This distinct phenotype may be responsible for the reduced immunosuppressive property of ectopic MSCs and may be associated with the pathogenesis of endometriosis. © The Japanese Society for Immunology. 2014. All rights reserved. For permissions, please e-mail:
    International Immunology 11/2014; 27(4). DOI:10.1093/intimm/dxu103