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.

Current impact factor: 2.75

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.754
2012 Impact Factor 2.767
2011 Impact Factor 2.471
2010 Impact Factor 2.138
2009 Impact Factor 2.813
2008 Impact Factor 2.525
2007 Impact Factor 2.887
2006 Impact Factor 2.033
2005 Impact Factor 1.49
2004 Impact Factor 1.392
2003 Impact Factor 1.052
2002 Impact Factor 0.921
2001 Impact Factor 1.169
2000 Impact Factor 1.204
1999 Impact Factor 1.232
1998 Impact Factor 1.082
1997 Impact Factor 1.133
1996 Impact Factor 1.608
1995 Impact Factor 1.257
1994 Impact Factor 1.308
1993 Impact Factor 1.417
1992 Impact Factor 1.053

Impact factor over time

Impact factor
Year

Additional details

5-year impact 2.51
Cited half-life 5.80
Immediacy index 0.47
Eigenfactor 0.01
Article influence 0.79
Website Autoimmunity website
ISSN 1607-842X
OCLC 300118157
Material type Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Informa Healthcare

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • On author's personal website or institution website
    • Publisher copyright and source must be acknowledged
    • On a non-profit server
    • Must link to publisher version
    • Publisher's version/PDF cannot be used
    • NIH funded authors may post articles to PubMed Central for release 12 months after publication
    • Wellcome Trust authors may deposit in Europe PMC after 6 months
  • Classification
    ​ yellow

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Aberrant T lymphocytes signaling is considered to play a crucial role in the abnormal immune state of primary immune thrombocytopenia (ITP). Lipid raft has been verified to engage in the T cell receptor (TCR)-mediated T lymphocytes signal transduction. Whether lipid raft-associated T cells signal transduction has impact on the pathogenesis of ITP is still unconfirmed. In this study, we aimed to reveal the abnormality in structure and function of lipid rafts (LRs) in CD4(+) and CD8(+) T lymphocytes of patients with ITP. Our results showed that there was an increased lipid raft aggregation in ITP patients, while this kind of increase would not be influenced by platelet counts or therapeutic regimes. Stimulation by anti-CD3/CD28 monoclonal antibodies promoted enhanced lipid raft clustering in T lymphocytes of ITP patients compared with negative controls. Methyl-β-cyclodextrin (MβCD) could block the abnormal lipid raft aggregation and disrupt the TCR-mediated T cells proliferation and cytokines secretion, including both proinflammatory cytokines and anti-inflammatory cytokines. The spontaneous activation of T lymphocytes from ITP patients might be due to the elevated co-localization of protein tyrosine phosphatase (PTP) CD45 and lipid rafts in patients' CD4(+) and CD8(+) T lymphocytes. These findings suggest that the autoactivation of T lymphocytes from ITP patients may lead to the abnormality in lipid raft structure and raft-anchored proteins, and the changes conversely promote the TCR-mediated T cells activation of ITP patients.
    Autoimmunity 08/2015; DOI:10.3109/08916934.2015.1070837
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    ABSTRACT: MicroRNAs (miRNAs) are short non-coding RNAs that play an important role in post-transcriptional regulation of gene expression. The past studies showed that miR-150 might emerge as a master regulator of gene expression during the immune cells differentiation and immune response process. Its regulation ability in immune cellular process might contribute to the host defense against invading pathogens, and dysregulated expression of miR-150 in immune cells might result in autoimmune diseases. This review summarized that miR-150 could regulate B cells, T cells and NK/iNKT cells differentiation and immune response. And also, this review provides a comprehensive view on the association of miR-150 and autoimmune diseases such as systemic sclerosis (SSc), multiple sclerosis, rheumatoid arthritis, systemic lupus erythematosus and contact sensitivity. Especially, the duplex role of miR-150 in the fibrosis process might contribute to the pathomechanism of SSc. Though much remains to be explored about the roles of miR-150 in pathogenic infection and autoimmune diseases, targeting miR-150 may serve as a promising therapy strategy.
    Autoimmunity 08/2015; DOI:10.3109/08916934.2015.1072518
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    ABSTRACT: Myasthenia gravis (MG) is a neuromuscular autoimmune disease, where antibodies against the acetylcholine receptor destroy this receptor. The role of thymectomy in the treatment of MG remains controversial. Because of the frequent association with other autoimmune diseases, we hypothesized that patients with multiple autoantibodies (autoAbs) might have a lower chance of reaching complete stable remission after thymectomy. We analyzed sera of 85 MG patients who underwent a thymectomy between April 2004 and December 2012. We used four different immunodot kits (D-Tek, Mons, Belgium): ANA25 Quantrix, Synthetase 10 Diver, Myositis 7 Diver and Liver 10 profile Diver, all automatized on the BlueDiver Instrument (D-Tek). The Myasthenia Gravis Foundation of America (MGFA) postintervention status was used to determine the outcome after thymectomy. AutoAbs other than anti-acetylcholine receptor (AChR) antibodies were detected in 29.4% of the patients of whom 16.5% clinically had a second autoimmune disease. In none of the seronegative patients other autoAbs were detected. No significant difference was observed in the 3-years remission rate after thymectomy in patients with or without antibodies other than anti-AChR antibodies. Although these autoAbs do not predict outcome in our MG patient cohort, screening for multiple autoAbs in MG patients might be warranted to identify patients with additional autoimmune diseases.
    Autoimmunity 07/2015;
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    ABSTRACT: Inflammasome is the cytoplasmic complex responsible for pro-IL1 β cleavage and secretion of IL-1β. Recently our group reported the first association between polymorphisms in the inflammasome receptor NLRP1 and adult-onset systemic lupus erythematosus (SLE) "di per se" and especially in SLE-associated renal disease, suggesting the involvement of NLRP1-inflammasome in the immune dysregulation characteristic of SLE patients. Considering that juvenile-onset SLE (JSLE) is more severe than adult SLE, and that the genetic background plays a major role in the early development of autoimmune diseases, we analysed selected polymorphisms in inflammasome genes (NLRP1, NLRP3, CARD8, IL1B, TNFAIP3) of children and adolescents with JSLE (n = 90) and in healthy controls (n = 144). A single polymorphism in IL1B, and not NLRP1, gene resulted in association with JSLE, suggesting that IL-1 β is involved in the pathogenesis of SLE, but different genes could play specific role in adult- or early-onset disease.
    Autoimmunity 07/2015; DOI:10.3109/08916934.2015.1064399
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    ABSTRACT: Progression to chronic renal failure varies between patients with lupus nephritis. We compared the effects of mycophenolate mofetil (MMF) and cyclophosphamide (CTX), on renal histology and cellular pathways of fibrosis in murine lupus nephritis. Female NZBWF1/J mice were randomized to treatment with vehicle, methylprednisolone (MP) alone, MMF + MP or CTX + MP for up to 12 weeks, and the effects on clinical parameters, renal histology, and fibrotic processes were investigated. Treatment with MMF + MP or CTX + MP both improved survival, renal function, and decreased anti-dsDNA antibody level and immune complex deposition in kidneys of mice with active nephritis. Vehicle-treated mice showed progressive increase in mesangial proliferation, inflammatory cell infiltration and renal tubular atrophy, associated with PKC-α activation, increased TGF-β1 expression and increased matrix protein deposition. MP treatment alone did not have any significant effect. MMF + MP or CTX + MP treatment for 12 weeks reduced these abnormalities. MMF + MP was more effective than CTX + MP in suppressing fibrotic mediators, histological fibrosis score and expression of TGF-β1, fibronectin and collagen I in the kidney. Results from in vitro experiments on human mesangial cells (HMC) showed that mycophenolic acid (MPA) was more effective than CTX in suppressing PKC-α activation and TGF-β1 secretion induced by human polyclonal anti-dsDNA antibodies. While both MPA and CTX decreased TGF-β1- and TNF-α-induced fibronectin synthesis, only MPA decreased IL-6 induced fibronectin synthesis. MPA and CTX show distinct effects on fibrotic and inflammatory processes in NZBWF1/J murine lupus nephritis, suggesting that MMF + MP may be more effective than CTX + MP in preserving normal renal histology in lupus nephritis.
    Autoimmunity 06/2015; DOI:10.3109/08916934.2015.1054027
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    ABSTRACT: In the past, there were no studies to evaluate the incidence of Sjogren's syndrome and its relationship with sex and age in patients with systemic sclerosis. In this study, we enrolled 2217 patients with systemic sclerosis and 6485 controls from Taiwan's Registry of Catastrophic Illness database and National Health Insurance Research Database. Every patient with systemic sclerosis was matched to at most three controls by sex, age, month, and year of first diagnosis of systemic sclerosis. Standardized incidence ratio (SIR) of Sjogren's syndrome in patients with systemic sclerosis and 95% confidence interval (95% CI) were calculated. Cox hazard regression was used to calculate the hazard ratio (HR). Both male and female patients with systemic sclerosis had higher incidences of Sjogren's syndrome (SIR: 7.59, 95% CI = 2.97-19.51; SIR: 7.59, 95% CI = 5.56-10.42, respectively). The incidence of Sjogren's syndrome in patients with systemic sclerosis was still higher compared with control when stratified according to age. Age at diagnosis of Sjogren's syndrome was earlier in patients with systemic sclerosis in both male and female groups (p = 0.018; p < 0.001, respectively). Systemic sclerosis was associated with Sjogren's syndrome after adjusting for age, sex, and various autoimmune diseases (HR: 5.98, 95% CI = 4.79-7.47, p < 0.001). Common cytokines, overlapping antibodies, and similar risk alleles were all potential causes of increased incidence of Sjogren's syndrome in systemic sclerosis.
    Autoimmunity 05/2015; DOI:10.3109/08916934.2015.1045583
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    ABSTRACT: Blockade of the complement cascade at the C5a/C5a receptor (C5aR)-axis is believed to be an attractive treatment avenue in rheumatoid arthritis (RA). However, the effects of such interventions during the early phases of arthritis remain to be clarified. In this study we use the murine delayed-type hypersensitivity arthritis (DTHA) model to study the very early effects of a blocking, non-depleting anti-C5aR mAb on joint inflammation with treatment synchronised with disease onset, an approach not previously described. The DTHA model is a single-paw inflammatory arthritis model characterised by synchronised and rapid disease onset driven by T-cells, immune complexes and neutrophils. We show that a reduction in paw swelling, bone erosion, cartilage destruction, synovitis and new bone formation is apparent as little as 60 h after administration of a single dose of a blocking, non-depleting anti-mouse C5aR mAb. Importantly, infiltration of neutrophils into the joint and synovium is also reduced following a single dose, demonstrating that C5aR signalling during the early stage of arthritis regulates neutrophil infiltration and activation. Furthermore, the number of T-cells in circulation and in the draining popliteal lymph node is also reduced following a single dose of anti-C5aR, suggesting that modulation of the C5a/C5aR axis results in effects on the T cell compartment in inflammatory arthritis. In summary, these data demonstrate that blockade of C5aR leads to rapid and significant effects on arthritic disease development in a DTHA model strengthening the rationale of C5aR-blockade as a treatment strategy for RA, especially during the early stages of arthritis flare.
    Autoimmunity 04/2015; DOI:10.3109/08916934.2015.1031888
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    ABSTRACT: Systemic lupus erythematosus (SLE) is a complicated autoimmune disease of multifactorial pathoaetiology. One of the most serious manifestations is lupus nephritis. The pathogenesis of SLE has not been well elucidated, but it has been reported that interleukin-17 (IL-17) and Th17 cells play important roles in the pathogenesis of SLE. IL-17A, a member of IL-17 family, amplifies the immune response by inducing the local production of chemokines and cytokines, recruiting neutrophils and monocytes, augmenting the production of autoantibodies, and aggravating the inflammation and damage of target organs such as the kidney in SLE. In recent years, several IL-17A pathway inhibitors have advanced into clinical trials, including the anti-IL-17A monoclonal antibody and the anti-17RA monoclonal antibody. Several agents have shown great success in Phase II trials in multiple autoimmune diseases such as psoriasis, rheumatoid arthritis, ankylosing spondylitis, multiple sclerosis, and non-infectious uveitis, which has sparked the urgent need of anti-IL-17A as innovative therapeutic option in controlling disease activity of moderate-to-severe SLE. Here, we review and summarize current progress in IL-17A and SLE from in vitro studies, human expression studies, and animal models, providing novel insight into its therapeutic potential.
    Autoimmunity 04/2015; DOI:10.3109/08916934.2015.1037441
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    ABSTRACT: A potential role of preproghrelin polymorphisms on autoimmune thyroid diseases (AITDs) has not been established equivocally yet. To estimate the association of two polymorphisms of preproghrelin gene with the predisposition to Graves' disease (GD) and Hashimoto's thyroiditis (HT) in children. The study was performed in 145 patients with GD, 87 with HT and 161 healthy volunteers. The two single nucleotide polymorphisms (SNPs) rs696217 (C_3151003_20) and rs4684677 (C_25607748_10) in the preproghrelin gene were genotyped by TaqMan SNP genotyping assay using the real-time PCR. Rs4684677 T alleles were more frequent in HT patients (99% in women and 100% in men) in comparison to healthy subjects (p = 0.002) with OR = 8.0 and 95% confidence interval for OR: 1.8-206.7. In women group, rs4684677 T alleles were more frequent compared to healthy controls (99%) in HT (p = 0.02) with OR = 6.7 and 95% confidence interval for OR: 1.2-168.37. Frequency of the SNP rs696217 did not differ between the groups. There was a significant relationship between rs696217 polymorphisms and anti-TSHR antibodies level (p = 0.036) in women from GD/HT groups. A significant relationship between rs696217 polymorphisms and anti-TG antibodies level in GD women group (p = 0.038) and between rs696217 polymorphisms and fT4 concentration (p = 0.03) were found. Rs4684677 T/A polymorphisms in preproghrelin gene could contribute to development of AITDs in children and T allele is the main risk factor.
    Autoimmunity 04/2015; DOI:10.3109/08916934.2015.1033687
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    ABSTRACT: We evaluated the co-occurrence of autoimmune diseases (ADs) in a large population of myasthenia gravis (MG) patients from a single center. Our survey included 984 patients, 904 with anti-acetylcholine receptor antibodies and 80 with anti-muscle specific kinase antibodies. The anti-acetylcholine receptor positive population included patients with early-onset (age at onset ≤50 years), late-onset and thymoma-associated disease. Follow-up ranged 2-40 years. Two-hundred and fourteen ADs were diagnosed in 185 patients; 26 of them had two or more ADs in association with MG. Thyroid disorders were the most common and, together with vitiligo and thrombocytopenia, occurred in all disease subsets. Otherwise, there was a broad variability with partial overlap among patient groups. The highest rate of ADs was observed in early-onset patients, while clusters, i.e. 2 or more ADs other than MG in the same individual, were more common among thymoma cases. Thirty-four diseases were diagnosed at the same time, 88 occurred before and 92 after the onset of MG. On multivariate analysis, immunosuppressive treatment was the only independent variable which negatively influenced the risk of developing other ADs in our cohort.
    Autoimmunity 04/2015; DOI:10.3109/08916934.2015.1031890
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    ABSTRACT: The immune system is known to affect reproductive function, and maternal-fetal immune tolerance is essential for a successful pregnancy. To investigate the relationship between autoimmune disease and female reproductive function, we performed a comparative analysis of the ovarian phenotypes for C57BL/6 mice, autoimmune disease-prone MRL/MpJ (MRL/+) mice and congenic MRL/MpJ-Fas(lpr) (MRL/lpr) mice harboring a mutation in the Fas gene that speeds disease onset. Both MRL-background strains showed earlier vaginal opening than C57BL/6 mice. The estrous cycle became irregular by 6 and 12 months of age in MRL/lpr mice and mice of the other two strains, respectively. Histological analysis at 3 months revealed that the number of primordial follicles was smaller in MRL-background mice than in C57BL/6 mice after 3 months. In addition, MRL/lpr and MRL/+ mice displayed lower numbers of ovarian follicles and corpora lutea at 3 and 6 months, and 6 and 12 months, respectively, than that in age-matched C57BL/6 mice. MRL/lpr and MRL/+ mice developed ovarian interstitial glands after 3 and 6 months, respectively. In particular, MRL/lpr mice showed numerous infiltrating lymphocytes within the ovarian interstitia, and partially stratified ovarian surface epithelia with more developed microvilli than that observed in C57BL/6 mice at 6 months. No significant differences in serum hormone levels were observed between the strains. In conclusion, MRL/lpr mice display altered ovarian development, morphology and function consistent with the progression of severe autoimmune disease, as these findings are less severe in MRL/+ counterparts.
    Autoimmunity 04/2015; DOI:10.3109/08916934.2015.1031889
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    ABSTRACT: Important interactions between female reproduction and autoimmunity are suggested by the female-predominance of systemic lupus erythematosus (SLE) and other autoimmune diseases and the amelioration of certain autoimmune diseases during pregnancy. Sexually dimorphic risk of developing SLE involves modulation of genetic risk by environmental factors, sex hormones and non-hormonal factors encoded on the sex chromosomes. In some lupus models, estrogen, via estrogen receptor alpha (ER-α), enhances production of highly pathogenic IgG2a/c autoantibodies (autoAbs). Some studies indicate that treatment with progesterone, a chief female reproductive steroid, can suppress IgG2a/2c autoAb production. Little is known about how endogenous progesterone impacts lupus autoimmunity. To investigate this, we introduced a disruptive progesterone receptor (PR) gene mutation into lupus-prone mice and tracked the development of spontaneous IgG autoAbs. Here, we present evidence that PR can suppress the emergence of class-switched IgG2c autoAbs, suggesting that PR and ER-α counter-regulate a critical step in lupus autoimmunity. PR's control of IgG2c autoAb production correlates with alterations in the relative abundance of splenic T follicular helper (TFH) cells and non-TFH CD4(+) T cells, especially regulatory T cells (TREGS). Surprisingly, PR also appears to help to maintain sexually dimorphic abundance of splenic leukocytes, a feature common to many mouse models of SLE. Together our results identify a novel molecular link between female reproduction and lupus autoimmunity. Further investigation into the immunomodulatory functions of PR promises to inform reproductive health care in women and offers mechanistic insight into important immunologic phenomena of pregnancy.
    Autoimmunity 04/2015; DOI:10.3109/08916934.2015.1030613
  • Autoimmunity 04/2015; DOI:10.3109/08916934.2015.1030922