Autoimmunity (Autoimmunity)

Publisher: Informa Healthcare

Journal description

Current understanding of autoimmune disease is being increasingly underpinned by the new molecular sciences. Progress in this area has been little short of spectacular, and all clinical specialities now recognise autoimmunity as a major component of the diseases with which they are involved. Autoimmunity is an international, peer reviewed journal that publishes articles of clinical and basic science on the pathogenesis, immunology, genetics, molecular biology, and treatment of autoimmune diseases. In addition to the basic mechanisms and elements of the immune system, the journal focuses on the autoimmune processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, diabetes, multiple sclerosis, and other systemic and organ-specific autoimmune diseases. The journal is not restricted to any disease type or clinical speciality, but reflects the areas where scientific progress is most rapid and clinical applications significant and widespread. The journal is valuable to clinicians and researchers in immunology and molecular biology.

RG Journal Impact: 2.62*

*This value is calculated using ResearchGate data and is based on average citation counts from work published in this journal. The data used in the calculation may not be exhaustive.

RG Journal impact history

2017 RG Journal impact Available summer 2018
2015 / 2016 RG Journal impact 2.62
2014 RG Journal impact 3.17
2013 RG Journal impact 3.05
2012 RG Journal impact 3.05
2011 RG Journal impact 3.13
2010 RG Journal impact 2.59
2009 RG Journal impact 3.87
2008 RG Journal impact 1.60

RG Journal impact over time

RG Journal impact

Additional details

Cited half-life 6.90
Immediacy index 0.80
Eigenfactor 0.00
Article influence 0.59
Website Autoimmunity website
ISSN 1607-842X
OCLC 300118157
Material type Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

This journal may support self-archiving.
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Publications in this journal

  • Article · Mar 2017 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: Systemic lupus erythematosus (SLE) is a polygenic pathological disorder which involves multiple organs. Self-specific B cells play a main role in the lupus pathogenesis by generating autoantibodies as well as by serving as important autoantigen-presenting cells. Autoreactive T lymphocytes, on the other hand, are responsible for B cell activation and proliferation, and cytokine production. Therefore, both factors promote the idea that a down-modulation of activated self-reactive T and B cells involved in the pathogenic immune response is a reasonable approach for SLE therapy. Annexin A1 (ANX A1) is expressed by many cell types and binds to phospholipids in a Ca(2+) dependent manner. Abnormal expression of ANX A1 was found on activated B and T cells in both murine and human autoimmunity, suggesting its potential role as a therapeutic target. While its role on T lymphocytes is through formyl peptide receptor-like molecules (FPRL), and the formed ANX A1/FPRL pathway modulates T cell receptor signalling, there is still no fool-proof data available for the role of ANX A1 in B cells. We employed a lupus model of Balb/c mice with pristane-induced SLE which very closely resembles human lupus. In the present study, we investigated the possibility to modulate the autoimmune response in a pristane-induced mouse model of SLE using an anti- ANX A1 antibody. Administration of this monoclonal antibody resulted in the inhibition of T-cell activation and proliferation, suppression of IgG anti-dsDNA antibody-secreting plasma cells and of proteinuria, decreased disease activity and prolonged survival compared to control group.
    Article · Mar 2017 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: Background and aims: Myeloid-derived suppressor cells (MDSCs) encompass a novel population of suppressor cells and a potential candidate for cell-based therapies in inflammatory diseases. Herein, we investigated their immunomodulatory properties in experimental inflammatory colitis and T cell-mediated immune responses in inflammatory bowel disease (IBD) patients. Methods: MDSCs (defined as CD14(-)HLA(-)DR(-/low)CD33(+)CD15(+)) numbers were determined in peripheral blood (PB) from IBD patients. PB MDSC function was assessed in vitro. Experimental colitis was induced upon 2,4,6-trinitrobenzene sulfonic acid (TNBS) treatment and MDSCs were characterized by flow cytometry. The in vivo suppressive potential of bone marrow (BM)-derived MDSCs (BM-MDSCs) was tested by using both depleting and adoptive transfer strategies. Results: MDSCs were enriched in the periphery of IBD patients during active disease. TNBS colitis induced amplification of MDSCs, particularly of the granulocytic (Ly6G(+)) subset during the effector phase of disease. Of interest, BM-MDSCs potently suppressed CD4(+ )T cell responses under steady state but failed to control colitis-associated immune responses in vivo. Mechanistically, under the colonic inflammatory milieu MDSCs switched phenotype (decreased proportion of Gr1(high) and increased numbers of Gr1(low)) and downregulated CCAAT/enhancer-binding protein beta (CEBPβ) expression, a critical transcription factor for the suppressive function of MDSCs. In accordance with the murine data, human CD33 (+) CD15(+ )MDSCs from peripheral blood of IBD patients not only failed to suppress autologous T cell responses but instead enhanced T cell proliferation in vitro. Conclusions: Our findings demonstrate an aberrant function of MDSCs in experimental inflammatory colitis and in IBD-associated immune responses in vitro. Delineation of the mechanisms that underlie the loss of MDSCs function in IBD may provide novel therapeutic targets.
    Article · Mar 2017 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: To determine the pathogenic role of adipokines, such as adiponectin and leptin, in rheumatoid arthritis (RA) by investigating whether serum levels of these adipokines correlated with disease activity in RA patients. Medline, Cochrane, EMBASE and Google Scholar were searched for studies published until 5 November 2015 reporting serum levels of leptin and adiponectin and measures of disease activity including DAS scores and radiographic progression scores (such as total change in SHS scores and number of erosions). Secondary outcomes included pain scores, functional status and health questionnaires. Only randomized controlled trials, cohort studies, or two-armed prospective or retrospective studies were included. A χ(2)-based test of homogeneity was performed using Cochran's Q statistic and I(2). A total of 917 predominantly female participants (average age range, 39-56 years) from six prospective cohort studies were included for assessment. A fixed-effects analysis was applied for leptin levels due to lack of heterogeneity among the studies (Q = 4.4364; I(2 )=( )32.38). A random-effects analysis was applied to serum levels of adiponectin because of significant heterogeneity between studies (Q = 4.444, I(2 )=( )77.50%). Serum leptin levels were higher in RA patients with high disease activity (pooled SMD: 0.53, 95% CI: 0.24-0.82); however, serum adiponectin levels did not correlate with RA disease activity (pooled OR: 1.38, 95% CI: 0.77-2.47). The meta-analysis provides an additional factor to determine high disease activity index in RA, that is, serum leptin levels, which can be of benefit when choosing treatment strategies.
    Article · Sep 2016 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: Distinct cellular level of the Ca(2+)-binding chaperone calreticulin (CRT) is essential for correct embryonal cardiac development and postnatal function. However, CRT is also a potential autoantigen eliciting formation of antibodies (Ab), whose role is not yet clarified. Immunization with CRT leads to cardiac injury, while overexpression of CRT in cardiomyocytes induces dilated cardiomyopathy (DCM) in animals. Hence, we analysed levels of anti-CRT Ab and calreticulin in the sera of patients with idiopatic DCM and hypertrophic cardiomyopathy (HCM). ELISA and immunoblot using human recombinant CRT and Pepscan with synthetic, overlapping decapeptides of CRT were used to detect anti-CRT Ab. Serum CRT concentration was tested by ELISA. Significantly increased levels of anti-CRT Ab of isotypes IgA (p < 0.001) and IgG (p < 0.05) were found in patients with both DCM (12/34 seropositive for IgA, 7/34 for IgG) and HCM (13/38 seropositive for IgA, 11/38 for IgG) against healthy controls (2/79 for IgA, 1/79 for IgG). Titration analysis in seropositive DCM and HCM patients documented anti-CRT Ab detected at 1/1600 dilution for IgG and 1/800 for IgA (and IgA1) and at least at 1/200 dilution for IgA2, IgG1, IgG2 and IgG3. Pepscan identified immunogenic CRT epitopes recognized by IgA and IgG Ab of these patients. Significantly increased levels of CRT relative to healthy controls were found in sera of patients with HCM (p < 0.01, 5/19). These data extend the knowledge of seroprevalence of anti-CRT Ab and CRT, and suggest possible involvement of autoimmune mechanisms directed to CRT in some forms of cardiomyopathies, which are clinically heterogeneous.
    Article · Sep 2016 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: Objectives: Recent evidence has demonstrated that CD3ζ (also called CD247) play a vital role in multiple autoimmune diseases. In this study, we explored the association between CD247 gene single-nucleotide polymorphisms (SNPs) and rheumatoid arthritis (RA) in a Chinese Han population. We also evaluated the CD3ζ expression profile in peripheral blood mononuclear cells (PBMCs) from patients with RA and health controls. Methods: Three CD247 polymorphisms (rs704853, rs1214611 and rs858554) were studied in 612 patients with RA and 848 controls in a Chinese population. Genotyping was performed using the Fluidigm 192.24 Dynamic Array™ Integrated Fluidic Circuit (IFC). For gene expression study, CD3ζ mRNA levels of 36 patients with RA and 39 healthy individuals were assessed by real-time polymerase chain reaction (RT-PCR). Data were analyzed by SPSS 11.5 software. Results: A significant association between rs858554 polymorphism and RA was found under all genetic models (all p < 0.05). Moreover, we found the genotype distribution and allele frequency of rs858554 were significant associated with ACCP(+) and RF(+) phenotype as compare to health controls (all p < 0.05). Unfortunately, we did not detect any significant associations between rs704853, rs1214611 and RA susceptibility and autoantibody profiles (all p > 0.05). The gene expression assays showed that CD3ζ mRNA levels were downregulated in PBMCs of patients with RA when compared to healthy controls. Conclusions: Our results, the first reported for distinct Chinese populations, support a role of the CD247 gene in the susceptibility to RA. Further studies with more sample size are necessary to clarify the exact role of CD247 gene in the pathogenesis of RA.
    Article · Apr 2016 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: The specificities and cross-reactions of antibodies induced by citrulline- and homocitrulline-containing proteins may give implications on the role of citrulline- and homocitrulline-binding antibodies in the pathogenesis and progression of rheumatoid arthritis (RA). Here we use rabbits as an experimental model of antibody development in RA. Thirty-two animals were immunized with peptide antigens containing either homocitrulline or citrulline. The sera were tested for binding to CCP and MCV antigens and to peptide sequences related to carboxyterminal telopeptides of type I and II collagens and containing arginine, citrulline, or homocitrulline. The binding of CCP and MCV antigens to antisera against homocitrulline-containing immunogens could be inhibited by human serum albumin containing homocitrulline, whereas similar binding to sera against citrulline-containing immunogens was not inhibited. The antisera induced with citrulline-containing collagen telopeptides recognized type I collagen-related antigens in a sequence-specific manner, as antibody binding to both citrulline- and homocitrulline-containing peptides was inhibited by corresponding citrullinated and native peptides. In contrast, type II collagen-related peptides were recognized by the antisera in a ureido group-specific manner, as their binding to homocitrulline-containing peptide was inhibited by both citrulline- and homocitrulline-containing, but not native peptide. Binding of the citrullinated type II collagen peptide could only be inhibited by the similarly citrullinated peptide. In conclusion, antibodies induced with citrulline or homocitrulline-containing antigens bound antigens in a ureido group-specific manner, recognizing citrulline and homocitrulline also in other sequences than those used in the original immunization. In competitive situations the amino acid present in the immunization antigen was favored.
    Article · Apr 2016 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: Studies suggest associations between the miR-146a single nucleotide polymorphisms (SNPs) and susceptibility to autoimmune diseases. However, the results are inconsistent and inconclusive. Therefore, the aim of this study was to arrive at a conclusion about the association between the three functional miR-146a SNPs and autoimmune disease risk. Studies were identified through PubMed/MEDLINE searches for studies published up to January 2016 using as keywords rs2910164, rs57095329, rs2431697, and miR-146a polymorphisms. Thirty studies were included in the meta-analysis. The SNP rs2910164 G > C was found to be associated with increased risk of multiple sclerosis (CC + CG versus GG, OR = 1.25, 95% CI: 1.01-1.55), with decreased risks of psoriasis (C versus G, OR = 0.81, 95% CI: 0.69-0.96; CC versus GC + GG, OR = 0.73, 95% CI: 0.56-0.94), Behcet's disease (CC versus GC + GG, OR = 0.60, 95% CI: 0.50-0.73), asthma (C versus G, OR = 0.80, 95% CI: 0.69-0.93; CC versus GC + GG, OR = 0.65, 95% CI: 0.48-0.86), and uveitis (CC + CG versus GG, OR = 0.61, 95% CI: 0.49-0.77). The SNP rs2431697 C > T was found to be associated with an increased risk of SLE (T versus C, OR = 1.26, 95% CI: 1.15-1.38; TC + TT versus CC, OR = 1.28, 95% CI: 1.03-1.58; TT versus TC + CC, OR = 1.40, 95% CI: 1.21-1.62). The SNP rs57095329 A > G was found to be associated with an increased risk of SLE (G versus C, OR = 1.25, 95% CI: 1.17-1.35). The miR-146a SNPs rs2910164, rs57095329, rs2431697 are associated with susceptibility to certain autoimmune diseases. However, for other autoimmune diseases, they may be protective or insignificant.
    Article · Apr 2016 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: TMEVPG1 is a long noncoding RNA, which can promote Interferon gamma (IFNG) transcript as an enhancer. It has been reported that plasma IFNG concentration was elevated and partly due to dysregulation of micro RNAs in patients with primary immune thrombocytopenia (ITP). However, the effect of long noncoding RNA on IFNG expression in ITP is currently not well understood. To explore whether TMEVPG1 is involved in ITP, this study examined the TMEVPG1 expression and analyzed the association between TMEVPG1 transcript and IFNG expression in patients with ITP and healthy controls. The result showed that TMEVPG1 expression in peripheral blood mononuclear cells (PBMCs) from active ITP patients were lower than in that of healthy controls. Further activation for 24 h in vitro resulted in decreased TMEVPG1 while elevated IFNG mRNA and protein expressions in activated PBMCs compared with un-activated PBMCs both in ITP patients and healthy controls. However, TMEVPG1 and IFNG mRNA had same up-regulated tendency after short-time activation (1, 2 and 4 h) in healthy controls. In addition, we detected T helper 1 (Th1) cell associated transcription factors T-bet, STAT1 and STAT4 mRNA levels, and found T-bet mRNA expression was lower in PBMCs from ITP patient in remission compared with healthy controls. In conclusion, we speculated that TMEVPG1 could promote IFNG transcription, and IFNG over-expression negative feedback regulated on TMEVPG1 expression, which resulted in decreased TMEVPG1 in ITP patients.
    Article · Apr 2016 · Autoimmunity
  • [Show abstract] [Hide abstract] ABSTRACT: Primary immunodeficiences are often accompanied by autoimmune phenomena. IL-12 receptor deficiency is a well characterized primary immunodeficiency that leads to propensity to intracellular infections mainly with mycobacteria and Salmonella. We report on two patients with IL-12 receptor β1 deficiency that presented with autoimmune manifestations and photosensitivity dermatitis and describe possible pathogenetic mechanisms leading to development of clinically significant autoimmune phenomena.
    Article · Jan 2016 · Autoimmunity