The Journal of Immunology (J Immunol)

Publisher: American Association of Immunologists, American Association of Immunologists

Journal description

The JI publishes novel results in all areas of experimental immunology.

Current impact factor: 4.92

Impact Factor Rankings

2016 Impact Factor Available summer 2017
2014 / 2015 Impact Factor 4.922
2013 Impact Factor 5.362
2012 Impact Factor 5.52
2011 Impact Factor 5.788
2010 Impact Factor 5.745
2009 Impact Factor 5.646
2008 Impact Factor 6
2007 Impact Factor 6.068
2006 Impact Factor 6.293
2005 Impact Factor 6.387
2004 Impact Factor 6.486
2003 Impact Factor 6.702
2002 Impact Factor 7.014
2001 Impact Factor 7.065
2000 Impact Factor 6.834
1999 Impact Factor 7.145
1998 Impact Factor 7.166
1997 Impact Factor 6.937
1996 Impact Factor 7.296
1995 Impact Factor 7.412
1994 Impact Factor 7.383
1993 Impact Factor 7.065
1992 Impact Factor 6.723

Impact factor over time

Impact factor

Additional details

5-year impact 5.26
Cited half-life 8.60
Immediacy index 0.96
Eigenfactor 0.24
Article influence 2.02
Website The Journal of Immunology website
Other titles Journal of immunology (Baltimore, Md.: 1950: Online), The journal of immunology, JI
ISSN 1550-6606
OCLC 34394395
Material type Document, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

American Association of Immunologists

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print archiving may be considered prior publication
    • Post-print on personal website only
    • Post-print not allowed on Institutional Repository
    • Set statement must accompany article (see policy link)
    • If mandated by funding agency may deposit authors post-print in PubMed Central, 6 or 12 months after publication
    • Papers submitted after 29th March 2011, funded by NIH, HHMI, MRC or Wellcome Trust, will be automatically deposited in PubMed Central if requested at submission
    • Publisher's version/PDF may only be used, if part of a thesis/ dissertation within a thesis repository
    • Must link to publisher version
  • Classification

Publications in this journal

  • [Show abstract] [Hide abstract] ABSTRACT: Despite decades of research, malaria remains a global health crisis. Current subunit vaccine approaches do not provide efficient long-term, sterilizing immunity againstPlasmodiuminfections in humans. Conversely, whole parasite vaccinations with their larger array of target Ags have conferred long-lasting sterilizing protection to humans. Similar studies in rodent models of malaria reveal that CD8(+)T cells play a critical role in liver-stage immunity after whole parasite vaccination. However, it is unknown whether all CD8(+)T cell specificities elicited by whole parasite vaccination contribute to protection, an issue of great relevance for enhanced subunit vaccination. In this article, we show that robust CD8(+)T cell responses of similar phenotype are mounted after prime-boost immunization againstPlasmodium bergheiglideosome-associated protein 5041-48-, sporozoite-specific protein 20318-325-,thrombospondin-related adhesion protein (TRAP) 130-138-, or circumsporozoite protein (CSP) 252-260-derived epitopes in mice, but only CSP252-260- and TRAP130-138-specific CD8(+)T cells provide sterilizing immunity and reduce liver parasite burden after sporozoite challenge. Further, CD8(+)T cells specific to sporozoite surface-expressed CSP and TRAP proteins, but not intracellular glideosome-associated protein 50 and sporozoite-specific protein 20, efficiently recognize sporozoite-infected hepatocytes in vitro. These results suggest that: 1) protection-relevant antigenic targets, regardless of their immunogenic potential, must be efficiently presented by infected hepatocytes for CD8(+)T cells to eliminate liver-stagePlasmodiuminfection; and 2) proteins expressed on the surface of sporozoites may be good target Ags for protective CD8(+)T cells.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: Cytokine-like 1 (CYTL1) is a novel potential cytokine that was first identified in CD34(+)cells derived from bone marrow and cord blood, and it was also found using our immunogenomics strategy. The immunobiological functions of CYTL1 remain largely unknown, and its potential receptor(s) has not been identified. A previous proposed hypothesis suggested that CYTL1 had structural similarities with CCL2 and that CCR2 was a potential receptor of CYTL1. In this study, we verify that CYTL1 possesses chemotactic activity and demonstrate that its functional receptor is CCR2B using a series of experiments performed in HEK293 cells expressing CCR2B or CCR2B-EGFP, including chemotaxis, receptor internalization, and radioactive binding assays. CYTL1 chemoattracts human monocytes but not PBLs, and its chemotactic activity toward monocytes is dependent on the CCR2B-ERK pathway. Furthermore, both human and mouse recombinant CYTL1 protein have chemotactic effects on macrophages from wild-type mice but not fromCcr2(-/-)mice. Furthermore, the chemotactic activity of CYTL1 is sensitive to pertussis toxin. All of the above data confirm that CCR2B is a functional receptor of CYTL1.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: The scaffold molecule POSH is crucial for the regulation of proliferation and effector function in CD8(+)T cells. However, its role in CD4(+)T cells is not known. In this study, we found that disruption of the POSH scaffold complex established a transcriptional profile that strongly skewed differentiation toward Th2, led to decreased survival, and had no effect on cell cycle entry. This is in stark contrast to CD8(+)T cells in which POSH regulates cell cycle and does not affect survival. Disruption of POSH in CD4(+)T cells resulted in the loss of Tak1-dependent activation of JNK1/2 and Tak1-mediated survival. However, in CD8(+)T cells, POSH regulates only JNK1. Remarkably, each type of T cell had a unique composition of the POSH scaffold complex and distinct posttranslational modifications of POSH. These data indicate that the mechanism that regulates POSH function in CD4(+)T cells is different from CD8(+)T cells. All together, these data strongly suggest that POSH is essential for the integration of cell-type-specific signals that regulate the differentiation, survival, and function of T cells.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: Helicobacter pyloriinfection causes chronic gastritis and peptic ulceration.H. pylori-initiated chronic gastritis is characterized by enhanced expression of many NF-κB-regulated inflammatory cytokines. Brd4 has emerged as an important NF-κB regulator and regulates the expression of many NF-κB-dependent inflammatory genes. In this study, we demonstrated that Brd4 was not only actively involved inH. pylori-induced inflammatory gene mRNA transcription but alsoH. pylori-induced inflammatory gene enhancer RNA (eRNA) synthesis. Suppression ofH. pylori-induced eRNA synthesis impairedH. pylori-induced mRNA synthesis. Furthermore,H. pyloristimulated NF-κB-dependent recruitment of Brd4 to the promoters and enhancers of inflammatory genes to facilitate the RNA polymerase II-mediated eRNA and mRNA synthesis. Inhibition of Brd4 by JQ1 attenuatedH. pylori-induced eRNA and mRNA synthesis for a subset of NF-κB-dependent inflammatory genes. JQ1 also inhibitedH. pylori-induced interaction between Brd4 and RelA and the recruitment of Brd4 and RNA polymerase II to the promoters and enhancers of inflammatory genes. Finally, we demonstrated that JQ1 suppressed inflammatory gene expression, inflammation, and cell proliferation inH. pylori-infected mice. These studies highlight the importance of Brd4 inH. pylori-induced inflammatory gene expression and suggest that Brd4 could be a potential therapeutic target for the treatment ofH. pylori-triggered inflammatory diseases and cancer.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: In chronic lymphocytic leukemia (CLL), the increment in PBLs is slower than the expected increment calculated from the cells' proliferation rate, suggesting that cellular proliferation and apoptosis are concurrent. Exploring this phenomenon, we found overexpression of caspase-3, higher cleaved poly (ADP-ribose) polymerase levels (p< 0.007), and a higher apoptosis rate in cells from patients with high counts compared with cells from patients with low counts. Although we previously found that STAT3 protects CLL cells from apoptosis, STAT3 levels were significantly higher in cells from patients with high counts than in cells from patients with low counts. Furthermore, overexpression of STAT3 did not protect the cells. Rather, it upregulatedcaspase-3and induced apoptosis. Remarkably, putative STAT3 binding sites were identified in thecaspase-3promoter, and a luciferase assay, chromatin immunoprecipitation, and an EMSA revealed that STAT3 activatedcaspase-3 However, caspase-3 levels increased only when STAT3 levels were sufficiently high. Using chromatin immunoprecipitation and EMSA, we found that STAT3 binds with low affinity to thecaspase-3promoter, suggesting that at high levels, STAT3 activates proapoptotic mechanisms and induces apoptosis in CLL cells.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: Fc receptor-like (FCRL) 5 is a novel IgG binding protein expressed on B cells, with the capacity to regulate Ag receptor signaling. We assessed FCRL5 expression on circulating B cells from healthy donors and found that FCRL5(+)cells are most enriched among atypical CD21(-/lo)/CD27(-)tissue-like memory (TLM) B cells, which are abnormally expanded in several autoimmune and infectious diseases. Using multicolor flow cytometry, FCRL5(+)TLM cells were found to express more CD11c and several inhibitory receptors than did the FCRL5(-)TLM subset. The homing receptor profiles of the two TLM subsets shared features consistent with migration away from lymphoid tissues, but they also displayed distinct differences. Analysis of IgH V regions in single cells indicated that although both subsets are diverse, the FCRL5(+)subset accumulated significantly more somatic mutations. Furthermore, the FCRL5(+)subset had more switched isotype expression and more extensive proliferative history. Microarray analysis and quantitative RT-PCR demonstrated that the two TLM subsets possess distinct gene expression profiles, characterized by markedly different CD11c, SOX5, T-bet, and RTN4R expression, as well as differences in expression of inhibitory receptors. Functional analysis revealed that the FCRL5(+)TLM subset responds poorly to multiple stimuli compared with the FCRL5(-)subset, as reflected by reduced calcium mobilization and blunted cell proliferation. We propose that the FCRL5(+)TLM subset, but not the FCRL5(-)TLM subset, underwent Ag-driven development and is severely dysfunctional. The present study elucidates the heterogeneity of TLM B cells and provides the basis to dissect their roles in the pathogenesis of inflammatory and infectious diseases.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: Neurotensin (NT) via its receptor 1 (NTR1) modulates the development of colitis, decreases HIF-1α/PHD2 interaction, stabilizes and increases HIF-1α transcriptional activity, and promotes intestinal angiogenesis. HIF-1α induces miR-210 expression, whereas miR-210 is strongly upregulated in response to NT in NCM460 human colonic epithelial cells overexpressing NTR1 (NCM460-NTR1). In this study, we examined whether NT activates a NTR1-HIF-1α-miR-210 cascade using in vitro (NCM460-NTR1 cells) and in vivo (transgenic mice overexpressing [HIF-1α-OE] or lacking HIF-1α [HIF-1α-knockout (KO)] in intestinal epithelial cells and mice lacking NTR1 [NTR1-KO]) models. Pretreatment of NCM460-NTR1 cells with the HIF-1α inhibitor PX-478 or silencing of HIF-1α (small interfering HIF-1α) attenuated miR-210 expression in response to NT. Intracolonic 2,4,6-trinitrobenzenesulfonic acid (TNBS) administration (2-d model) increased colonic miR-210 expression that was significantly reduced in NTR1-KO, HIF-1α-KO mice, and wild-type mice pretreated intracolonically with locked nucleic acid anti-miR-210. In contrast, HIF-1α-OE mice showed increased miR-210 expression at baseline that was further increased following TNBS administration. HIF-1α-OE mice had also exacerbated TNBS-induced neovascularization compared with TNBS-exposed wild-type mice. TNBS-induced neovascularization was attenuated in HIF-1α-KO mice, or mice pretreated intracolonically with anti-miR-210. Intracolonic anti-miR-210 also reduced colitis in response to TNBS (2 d). Importantly, miR-210 expression was increased in tissue samples from ulcerative colitis patients. We conclude that NT exerts its proinflammatory and proangiogenic effects during acute colitis via a NTR1-prolyl hydroxylase 2/HIF-1α-miR-210 signaling pathway. Our results also demonstrate that miR-210 plays a proinflammatory role in the development of colitis.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: IL-17-producing CD4(+)T cells (Th17 cells) regulate host defense and immune pathogenesis, and IL-6 plays an important role for the differentiation of Th17 cells. We have previously identified that TNFR-associated factor (TRAF)5 binds to the signal-transducing receptor gp130 through the C-terminal TRAF domain and inhibits Th17 development mediated by IL-6. Although gp130 has TRAF-binding motifs that can be recognized by other TRAF family proteins, it is unclear how TRAFs regulate IL-6-driven Th17 differentiation in general. Using retrovirus-mediated gene complementation and gene silencing approaches, we found that not only TRAF5 but also TRAF2 restrained the IL-6R signaling, whereas TRAF1, TRAF3, TRAF4, and TRAF6 did not.Traf2silencing further promoted the ability of naive CD4(+)T cells fromTraf5(-/-)mice to differentiate into Th17 cells. Notably, TRAF5 but not TRAF2 expressed in naive CD4(+)T cells was rapidly downregulated after TCR triggering, which indicates that TRAF5 specifically inhibits instructive IL-6 signals in the initial stage of Th17 development. Collectively, our results demonstrate a dedicated role for TRAF2 and TRAF5 in the process of IL-6-mediated Th17 development and a differential role for TCR signaling in regulation of TRAF2 and TRAF5. Therefore, both TRAF2 and TRAF5 work as important regulators of the IL-6R signaling needed for Th17 development.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: Pannexin1 (Panx1) channels are large high conductance channels found in all vertebrates that can be activated under several physiological and pathological conditions. Our published data indicate that HIV infection results in the extended opening of Panx1 channels (5-60 min), allowing for the secretion of ATP through the channel pore with subsequent activation of purinergic receptors, which facilitates HIV entry and replication. In this article, we demonstrate that chemokines, which bind CCR5 and CXCR4, especially SDF-1α/CXCL12, result in a transient opening (peak at 5 min) of Panx1 channels found on CD4(+)T lymphocytes, which induces ATP secretion, focal adhesion kinase phosphorylation, cell polarization, and subsequent migration. Increased migration of immune cells is key for the pathogenesis of several inflammatory diseases including multiple sclerosis (MS). In this study, we show that genetic deletion of Panx1 reduces the number of the CD4(+)T lymphocytes migrating into the spinal cord of mice subjected to experimental autoimmune encephalomyelitis, an animal model of MS. Our results indicate that opening of Panx1 channels in response to chemokines is required for CD4(+)T lymphocyte migration, and we propose that targeting Panx1 channels could provide new potential therapeutic approaches to decrease the devastating effects of MS and other inflammatory diseases.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: IL-21, a pleiotropic cytokine strongly linked with autoimmunity and inflammation, regulates diverse immune responses. IL-21 can be potently induced in CD4(+)T cells by IL-6; however, very little is known about the mechanisms underlying the transcriptional regulation of theIl21gene at the chromatin level. In this study, we demonstrated that a conserved noncoding sequence located 49 kb upstream of theIl21gene contains an enhancer element that can upregulateIl21gene expression in a STAT3- and NFAT-dependent manner. Additionally, we identified enhancer-blocking insulator elements in theIl21locus, which constitutively bind CTCF and cohesin. In naive CD4(+)T cells, these upstream and downstream CTCF binding sites interact with each other to make a DNA loop; however, theIl21promoter does not interact with anycis-elements in theIl21locus. In contrast, stimulation of CD4(+)T cells with IL-6 leads to recruitment of STAT3 to the promoter and novel distal enhancer region. This induces dynamic changes in chromatin configuration, bringing the promoter and the regulatory elements in close spatial proximity. The long-range interaction between the promoter and distal enhancer region was dependent on IL-6/STAT3 signaling pathway but was disrupted in regulatory T cells, where IL-21 expression was repressed. Thus, our work uncovers a novel topological chromatin framework underlying proper transcriptional regulation of theIl21gene.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: Apoptotic debris, autoantibody, and IgG-immune complexes (ICs) have long been implicated in the inflammation associated with systemic lupus erythematosus (SLE); however, it remains unclear whether they initiate immune-mediated events that promote disease. In this study, we show that PBMCs from SLE patients experiencing active disease, and hematopoietic cells from lupus-prone MRL/lprand NZM2410 mice accumulate markedly elevated levels of surface-bound nuclear self-antigens. On dendritic cells (DCs) and macrophages (MFs), the self-antigens are part of IgG-ICs that promote FcγRI-mediated signal transduction. Accumulation of IgG-ICs is evident on ex vivo myeloid cells from MRL/lprmice by 10 wk of age and steadily increases prior to lupus nephritis. IgG and FcγRI play a critical role in disease pathology. Passive transfer of pathogenic IgG into IgG-deficient MRL/lprmice promotes the accumulation of IgG-ICs prior to significant B cell expansion, BAFF secretion, and lupus nephritis. In contrast, diminishing the burden IgG-ICs in MRL/lprmice through deficiency in FcγRI markedly improves these lupus pathologies. Taken together, our findings reveal a previously unappreciated role for the cell surface accumulation of IgG-ICs in human and murine lupus.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: Chronic lymphocytic leukemia (CLL) patients assigned to stereotyped subset #4 (mutated IGHV4-34/IGKV2-30 BCR Ig) display a particularly indolent disease course. Immunogenetic studies of the clonotypic BCR Ig of CLL subset #4 suggested a resemblance with B cells rendered anergic through chronic autoantigenic stimulation. In this article, we provide experimental evidence that subset #4 CLL cells show low IgG levels, constitutive ERK1/2 activation, and fail to either release intracellular Ca(2+)or activate MAPK signaling after BCR cross-linking, thus displaying a signature of B cell anergy at both biochemical and functional levels. Interestingly, TLR1/2 triggering restored BCR functionality, likely breaching the anergic state, and this was accompanied by induction of the miR-17∼92 cluster, whose members target critical BCR-associated molecules, including MAPKs. In conclusion, we demonstrate BCR anergy in CLL subset #4 and implicate TLR signaling and the miR-17∼92 cluster in the regulation of the anergic state. This detailed signaling profiling of subset #4 has implications for advanced understanding of the complex regulation of intracellular signaling pathways in CLL, currently a major therapeutic target of the disease.
    No preview · Article · Apr 2016 · The Journal of Immunology
  • [Show abstract] [Hide abstract] ABSTRACT: It has been suspected for many years that cattle possess two functional IgH gene loci, located onBos taurusautosome (BTA) 21 and BTA11, respectively. In this study, based on fluorescence in situ hybridization and additional experiments, we showed that all functional bovine IgH genes were located on BTA21, and only a truncated μCH2 exon was present on BTA11. By sequencing of seven bacterial artificial chromosome clones screened from a Hostein cow bacterial artificial chromosome library, we generated a 678-kb continuous genomic sequence covering the bovine IGHV, IGHD, IGHJ, and IGHC genes, which are organized as IGHVn-IGHDn-IGHJn-IGHM1-(IGHDP-IGHV3-IGHDn)3-IGHJn-IGHM2-IGHD-IGHG3-IGHG1-IGHG2-IGHE-IGHA. Although both of two functional IGHM genes, IGHM1 and IGHM2, can be expressed via independent VDJ recombinations, the IGHM2 can also be expressed through class switch recombination. Likely because more IGHD segments can be involved in the expression of IGHM2, the IGHM2 gene was shown to be dominantly expressed in most tissues throughout different developmental stages. Based on the length and identity of the coding sequence, the 23 IGHD segments identified in the locus could be divided into nine subgroups (termed IGHD1 to IGHD9). Except two members of IGHD9 (14 nt in size), all other functional IGHD segments are longer than 30 nt, with the IGHD8 gene (149 bp) to be the longest. These remarkably long germline IGHD segments play a pivotal role in generating the exceptionally great H chain CDR 3 length variability in cattle.
    No preview · Article · Apr 2016 · The Journal of Immunology