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: 2.71

Impact Factor Rankings

2015 Impact Factor Available summer 2016
2014 Impact Factor 2.714
2013 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

Additional details

5-year impact 2.16
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

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
    • Non-commercial
    • 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

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: We previously reported the importance of connective tissue growth factor (CTGF) in rheumatoid arthritis (RA). CTGF contains four distinct modules connected in tandem, namely insulin-like growth factor-binding protein (IGFBP)-like, von Willebrand factor (vWF) type C repeat, thrombospondin type 1 (TSP-1) repeat, and carboxyl-terminal (CT) modules. The relationships between each of these modules of CTGF and RA remain unknown. Here, we analyzed how inhibition of each CTGF module affects the pathophysiology of RA. We conducted stimulation and suppression experiments on synovial cells (MH7A) obtained from patients with RA. Moreover, we examined angiogenesis by means of a tube-formation assay performed using human umbilical vein endothelial cells (HUVECs), and we used tartrate-resistant acid phosphatase (TRAP) staining to analyze osteoclastogenesis. Our results showed that M-CSF/RANKL-mediated osteoclastogenesis was enhanced when CTGF was added, but the effect of CTGF was neutralized by mAbs against CTGF modules 1-4. Furthermore, CTGF treatment of HUVECs induced formation of tubular networks, which resulted in acceleration of the angiogenesis of RA synoviocytes, and quantification showed that this tubular-network formation was also disrupted by anti-CTGF module 1-4 mAbs. Lastly, TNF-α enhanced the expression of CTGF and matrix metalloproteinase-3 (MMP3) in MH7A cells, and this enhancement was potently neutralized by mAbs against CTGF modules 1, 3 and 4. Thus, our results indicate that not only a mAb against CTGF but also mAbs against each specific module of CTGF might serve as potential therapeutic agents in the treatment of RA.
    Autoimmunity 11/2015; DOI:10.3109/08916934.2015.1113405
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    ABSTRACT: This study compared the effects of different dosages of intravenous immunoglobulin (IVIg) against immune thrombocytopenia (ITP). A total of 167 patients, 91 adults and 76 children, with ITP, followed-up for three years in the case-control study, were divided into three subgroups according to the dosages of IVIg administered: group A (0.2 g/kg/day), group B (0.3 g/kg/day) and group C (0.4 g/kg/day). The therapeutic response in 91 adult patients did not differ significantly among the three groups of IVIg dosages (p = 0.459). The response rate of IVIg treatment in the three adult groups was 97.1% for group A, 97.2% for group B and 100% for group C. The mean time for raising platelets to 30 × 10(9)/L in group A was 2.5 days, group B 3.2 days and group C 2.9 days (p = 0.324). The median IVIg consumption in group A was 0.83 g/kg, group B 1.22 g/kg and group C 1.64 g/kg (p < 0.01). Similar results were shown in the children groups. The follow-up results showed no significant difference of clinical outcome between groups A, B and C. In conclusion, low-dose IVIg treatment is shown to be as effective as high-dose regimen without increasing the risk of developing the patients into chronic ITP conditions, suggesting that ITP patients could be treated more cost-effectively by lower conventional dosage of IVIg regimen.
    Autoimmunity 11/2015; DOI:10.3109/08916934.2015.1104671
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    ABSTRACT: Objective: To examine the possible role of IL-17A rs2275913, IL-17F rs763780 and rs2397084 polymorphisms as risk factors for pSLE in a cohort of Egyptian children and to investigate their association with the clinico-pathological features including lupus nephritis (LN). Methods: Typing of IL-17A and IL-17F polymorphisms was done using restriction fragment length polymorphism for 115 children with SLE and 259 age- and sex-matched healthy controls. Results: No significant differences were found between pSLE patients and healthy controls for the allele and genotype frequencies of IL-17A rs2275913, IL-17F rs763780 and rs2397084 (p > 0.05). However, the combined genotype GGAGAA and the haplotype GGA had significant association with pSLE (pc = 0.042 and <0.001, respectively). The AA genotype of IL-17F rs763780 is more frequent in female patients (p = 0.002) and the AA genotype of IL-17F rs2397084 is more associated with positivity of ds-DNA (p = 0.007). No more associations were found for the demographic and clinical data of pSLE patients including risk of LN development, risk of non-remission, overall survival, activity and chronicity indices. Conclusion: The GGAGAA combined genotype and the GGA haplotype of IL-17A rs2275913, IL-17F rs763780 and rs2397084 can be considered risk factors for the development of SLE in Egyptian children. IL-17A rs2275913, IL-17F rs763780 and rs2397084 are not related to the LN development, SLE disease activity or overall survival.
    Autoimmunity 10/2015; DOI:10.3109/08916934.2015.1101071
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    ABSTRACT: Background: Despite the frequently encountered association between thyroid disease and systemic lupus erythematosus (SLE) is well known, it is of surprise that only several reports compromised of small population size support this observation. Objectives: To investigate the association of comorbid SLE and hyperthyroidism. Methods: Using the database of the largest health maintenance organization (HMO) in Israel, the Clalit Health Services, we searched for the co-existence of SLE and hyperthyroidism. Patients with SLE were compared with age- and sex-matched controls regarding the prevalence of hyperthyroidism in a case-control study. Chi-square and t-tests were used for univariate analysis and a logistic regression model was used for multivariate analysis. Results: The study included 5018 patients with SLE and 25 090 age- and sex- matched controls. The prevalence of hyperthyroidism in patients with SLE was increased compared with the prevalence in controls (2.59% and 0.91%, respectively, p < 0.001). In a multivariate analysis, SLE was associated with hyperthyroidism (odds ratio 2.52, 95% confidence interval 2.028-3.137). Conclusions: Patients with SLE have a greater prevalence of hyperthyroidism than matched controls. Therefore, physicians treating patients with SLE should be aware of this possibility of this thyroid dysfunction.
    Autoimmunity 10/2015; DOI:10.3109/08916934.2015.1090985
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    ABSTRACT: Many studies have reported the association between the CARD8 gene polymorphism rs2043211 and the susceptibility to Crohn's disease (CD), but the results have remained quite contradictory. Therefore, the aim of the meta-analysis was to explore whether the CARD8 rs2043211 polymorphism has an effect on CD risk. We performed a systematic literature search for related articles published up to July 2014 in multiple databases. Six eligible articles containing eight studies were selected. Odds ratios (ORs) as well as their corresponding 95% confidence intervals (CIs) were used to estimate the association between the CARD8 polymorphism and CD risk in different genotypic models. Heterogeneity analysis was also performed and publication bias was taken into account. Subgroup analyses were conducted according to different ethnicities, as well as different types of CD. In the pooled analyses, no statistical significant association was found between the CARD8 polymorphism and CD risk in the overall population or Caucasian subgroup in the additive model (overall population: OR = 0.93, 95% CI = 0.87-1.01; Caucasian: OR = 0.93, 95% CI = 0.83-1.05). However, subgroup analysis based on different CD types showed a significant association between the CARD8 polymorphism and CD risk in the additive model (ileal CD: OR = 0.83, 95% CI = 0.70-0.98; stenotic or fistulizing CD: OR = 0.81, 95% CI = 0.72-0.92). Our results indicated that CD may involve different types of pathogenesis and have variable clinical manifestations. In patients with ileal, stenotic or fistulizing CD, the mutant-type rs2043211 polymorphism may generate a potentially protective effect.
    Autoimmunity 10/2015; DOI:10.3109/08916934.2015.1045581
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    ABSTRACT: Autoimmune diseases (AIDs) are chronic conditions initiated by the loss of immunological tolerance to self-antigens and represent a heterogeneous group of disorders that affect specific target organs or multiple organs in different systems. While the pathogenesis of AID remains unclear, its aetiology is multifunctional and includes a combination of genetic, epigenetic, immunological and environmental factors. In AIDs, several epigenetic mechanisms are defective including DNA demethylation, abnormal chromatin positioning associated with autoantibody production and abnormalities in the expression of RNA interference (RNAi). It is known that environmental factors may interfere with DNA methylation and histone modifications, however, little is known about epigenetic changes derived of regulation of RNAi. An approach to the known environmental factors and the mechanisms that alter the epigenetic regulation in AIDs (with emphasis in systemic lupus erythematosus, the prototype of systemic AID) are showed in this review.
    Autoimmunity 09/2015; DOI:10.3109/08916934.2015.1086996
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    ABSTRACT: The mechanisms underlying development of ribonucleoprotein (RNP) autoantibodies are unclear. The U1-70K protein is the predominant target of RNP autoantibodies, and the RNA binding domain has been shown to be the immunodominant autoantigenic region of U1-70K, although the specific epitopes are not known. To precisely map U1-70K epitopes, we developed silicon-based peptide microarrays with >5700 features, corresponding to 843 unique peptides derived from the U1-70K protein. The microarrays feature overlapping peptides, with single-amino acid resolution in length and location, spanning amino acids 110-170 within the U1-70K RNA binding domain. We evaluated the serum IgG of a cohort of patients with systemic lupus erythematosus (SLE; n = 26) using the microarrays, and identified multiple reactive epitopes, including peptides 116-121 and 143-148. Indirect peptide ELISA analysis of the sera of patients with SLE (n = 88) revealed that ∼14% of patients had serum IgG reactivity to 116-121, while reactivity to 143-148 appeared to be limited to a single patient. SLE patients with serum reactivity to 116-121 had significantly lower SLE Disease Activity Index (SLEDAI) scores at the time of sampling, compared to non-reactive patients. Minimal reactivity to the peptides was observed in the sera of healthy controls (n = 92). Competitive ELISA showed antibodies to 116-121 bind a common epitope in U1-70K (68-72) and the matrix protein M1 of human influenza B viruses. Institutional Review Boards approved this study. Knowledge of the precise epitopes of U1-70K autoantibodies may provide insight into the mechanisms of development of anti-RNP, identify potential clinical biomarkers and inform ongoing clinical trails of peptide-based therapeutics.
    Autoimmunity 09/2015; DOI:10.3109/08916934.2015.1077233
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    ABSTRACT: Type 1 diabetes mellitus (T1DM) is an autoimmune disease characterized by an autoimmune-mediated loss of insulin secreting β-cells. Each B lymphocyte clone that escapes immune tolerance produces a specific antibody. No specific treatment against autoantibodies is available for autoimmune diseases. We have developed a strategy to produce an antiserum against autoantibodies for the treatment of T1DM. Non-obese diabetic (NOD) but not Balb/c mouse serum contains autoantibodies. Antisera were produced by immunizing Balb/c mice with affinity-purified IgG from NOD or BALB/c mice along with the immune adjuvant (hereafter, NIgG or BIgG, respectively). A bolus administration of NIgG significantly reduced serum autoantibodies, autoantibody-positive B lymphocytes in the spleens of NOD mice, mortality and morbidity of diabetes, blood glucose and islet immune infiltration, whereas it increased islet mass in NOD mice for at least 26 weeks. NIgG antiserum treatment has no significant effect on CD3(+), CD4(+) or CD8(+) T cells and B220(+) or CD19(+) B cells. BIgG also imparted a moderate therapeutic effect, although it was considerably lower than that of NIgG. NIgG did not cross-react with allogeneic serum. NIgG showed no effect on Balb/c mice. The results show the feasibility of producing antiserum against autoantibodies to prevent and treat autoimmune-induced T1DM with a single bolus administration.
    Autoimmunity 09/2015; DOI:10.3109/08916934.2015.1079819
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    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; 48(7):1-4. 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; 48(7):1-17. 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; 48(7):1-7. DOI:10.3109/08916934.2015.1045583