Autoimmunity reviews

Publisher: Elsevier

Journal Impact: 10.13*

*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.

Journal impact history

2016 Journal impact Available summer 2017
2015 Journal impact 10.13
2014 Journal impact 9.17
2013 Journal impact 7.50
2012 Journal impact 7.62
2011 Journal impact 8.72
2010 Journal impact 6.11
2009 Journal impact 7.11

Journal impact over time

Journal impact

Additional details

Cited half-life 3.50
Immediacy index 2.98
Eigenfactor 0.02
Article influence 1.40
ISSN 1873-0183

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Publications in this journal

  • [Show abstract] [Hide abstract] ABSTRACT: The innovative medicine initiative project called PRECISESADS will study 2.500 individuals affected by systemic autoimmune diseases (SADs) and controls. Among extensive OMICS approaches, multi-parameter flow cytometry analyses will be performed in eleven different centers. Therefore, the integration of all data in common bioinformatical and biostatistical investigations requires a fine mirroring of all instruments. We describe here the procedure elaborated to achieve this prerequisite. One flow cytometer chosen as reference instrument fixed the mean fluorescence intensities (MFIs) of 8 different fluorochrome-conjugated antibodies (Abs) using VersaComp Ab capture beads. The ten other centers adjusted their own PMT voltages to reach the same MFIs. Subsequently, all centers acquired Rainbow 8-peak beads data on a daily basis to follow the stability of their instrument overtime. One blood sample has been dispatched and concomitantly stained in all centers. Comparison of leukocytes frequencies and cell surface marker MFIs demonstrated the close sensitivity of all flow cytometers, allowing a multicenter analysis. The effective multi-center harmonization enables the constitution of a workable wide flow cytometry database for the identification of specific molecular signatures in individuals with SADs.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: “The objective of Pitfall!™ is to guide Harry through a maze of jungle scenes, jumping over or avoiding many deadly dangers… Harry has three lives in each game.” If you exchange Harry's adventures with “Life with SLE,” patients have to be guided through the jungle having just one life and the deadly dangers are flares, organ manifestations, and, e.g., consequences of immunosuppressive medications, especially glucocorticoids. Monitoring and treatment in line with recommendations and guidelines may be supportive to survive the first 3 to 5 levels in most cases, but for higher levels of the reality game, creativity is needed and life becomes more risky. The aim of this reflection is to identify common pitfalls and to stimulate further research and collaboration in specific areas of the lupus jungle. Topics like “Hidden Power Unit,” “Looks similar …,” “Rev Meter for SLE,” “Flare Prediction,” “Level 2: Eminence Based,” “Lupus = Lifelong Immunosuppression?!,” “Glucocorticoids,” “Antimalarials Are Contraindicated,” “It Is All About Immunosuppression,” “Prediction of Damage,” and “Patient Global Assessment (PGA) versus Physician Global Assessment (PhGA)” are addressed. Raised ideas and thoughts are by no means complete or exclusive, but if taken up, they may hopefully lead to another approach in daily care and trials in SLE.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Type 1 diabetes (T1D) is an autoimmune disease characterized by the loss of pancreatic beta cells in the islets of Langerhans. Although genetic predisposition plays an important role in T1D development, studies of identical twins suggest that environmental factors such as viruses and other pathogens may be critical triggers either through direct cytolytic effect and gradual beta cell destruction, or by bystander activation of the immune system. In addition, viruses may circumvent the host immune response and have the capacity to establish chronic lifelong infections. The association of various viral infections with the induction of T1D has been extensively studied at the serological and epidemiological level. However, there is still little evidence from studies of human pancreas to confirm their presence or a causal role in disease pathogenesis. In this review, we identify possible suspects for viral triggers of disease and explain their potential roles in the “viral paradigm” of T1D.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Parkinson's disease is a neurodegenerative disease that causes the death of dopaminergic neurons in the substantia nigra. The resulting dopamine deficiency in the basal ganglia leads to a movement disorder that is characterized by classical parkinsonian motor symptoms. Parkinson's disease is recognized as the most common neurodegenerative disorder after Alzheimer's disease.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: HBsAg and HPV L1 proteins – the HBV and HPV antigens utilized in current vaccines – share amino acid sequences with human proteins such as cardiomyopathy-associated protein 5, titin, protein-arginine deiminase, E3 ubiquitin-protein ligase RNF19A, bassoon, G-protein coupled receptor for fatty acids, insulin isoform 2, and mitogen-activated protein kinase kinase kinase 10, inter alia. Many shared peptides are also part of immunopositive epitopes. The data 1) support the possibility of crossreactions between the two viral antigens and human proteins that, when altered, may associate with neuropsychiatric, cardiovascular and altered metabolic conditions such as multiple sclerosis, amyotrophic lateral sclerosis, diabetes, and sudden death; 2) confirm the concept that only vaccines based on sequences unique to pathogens might nullify potential crossreactivity risks in vaccination protocols.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: The crucial issue for a better pregnancy outcome in women with autoimmune rheumatic diseases is appropriate planning, with counseling of the ideal timing and treatment adaptation. Drugs used to treat rheumatic diseases may interfere with fertility or increase the risk of miscarriages and congenital abnormalities. MTX use post-conception is clearly linked to abortions as well as major birth defects, so it should be stopped 3months before conception. Leflunomide causes abnormalities in animals even in low doses. Although in humans, it does not seem to be as harmful as MTX, when pregnancy is detected in a patient on leflunomide, cholestyramine is given for washout. Sulfasalazine can be used safely and is an option for those patients who were on MTX or leflunomide. Azathioprine is generally the immunosuppressive of choice in many high-risk pregnancy centers because of the safety profile and its steroid-sparing property. Cyclosporine and tacrolimus can also be used as steroid-sparing agents, but experience is smaller. Although prednisone and prednisolone are inactivated in the placenta, we try to limit the dose to the minimal effective one, to prevent side effects. Antimalarials have been broadly studied and are safe during pregnancy and breastfeeding. Among biologic disease modifying anti-rheumatic agents (bDMARD), the anti-TNFs that have been used for longer are the ones with greater experience. The large monoclonal antibodies do not cross the placenta in the first trimester, and after conception, the decision to continue medication should be taken individually. The experience is larger in women with inflammatory bowel diseases, where anti-TNF is generally maintained at least until 30weeks to reduce fetal exposure. Live vaccines should not be administrated to the infant in the first 6months of life. Pregnancy data for rituximab, abatacept, anakinra, tocilizumab, ustekinumab, belimumab, and tofacitinib are limited and their use in pregnancy cannot currently be recommended.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Systemic sclerosis (SSc) is a multi-systemic autoimmune disease that mainly affects the skin, lungs, gastrointestinal tract, heart and kidneys. Pulmonary disease in patients with SSc is strongly associated with mortality. The mechanisms involved into its pathophysiology include the activation of autoimmune cells and hyperplasia of fibroblasts with an increased capacity to produce collagen and diminished collagen breakdown. Although pulmonary biopsy is the gold standard for the diagnosis of interstitial lung disease in SSc, the most commonly used method is high-resolution computed tomography due to its high sensitivity and specificity. Herein, a comprehensive review on the pulmonary involvement in SSc is presented highlighting the radiologic–pathologic correlations.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Women with recurrent pregnancy losses (RPL) and repeated implantation failures (RIF) have auto- and cellular immune abnormalities. Approximately, 20% of women with RPL have autoimmune abnormalities, particularly antiphospholipid antibodies (APA). In addition, these women have a higher prevalence of antinuclear antibody, anti-thyroperoxidase and anti-thyroglobulin antibodies, and other non-organ-specific autoantibodies. In women with RPL, the presence of autoimmunity is often associated with cellular immune abnormalities, such as increased NK cell levels and Th1/Th2 cell ratios. Vitamin D (VD) plays a major role in regulation of auto- and cellular immune abnormalities. VD deficiency is prevalent in women with RPL, and women with VD deficiency have increased auto- and cellular immune abnormalities as compared with women with normal VD levels. VD has immune regulatory effects on various immune effectors including T, B and NK cells. Potential therapeutic application of VD for RPL and RIF with auto- and cellular immune abnormalities should be explored.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: In an effort to find naturally occurring substances that reduce cholesterol by inhibiting 3-hydroxy-3-methylglutaryl-coenzyme A reductase (HMGCR), statins were first discovered by Endo in 1972. With the widespread prescription and use of statins to decrease morbidity from myocardial infarction and stroke, it was noted that approximately 5% of all statin users experienced muscle pain and weakness during treatment. In a smaller proportion of patients, the myopathy progressed to severe morbidity marked by proximal weakness and severe muscle wasting. Remarkably, Mammen and colleagues were the first to discover that the molecular target of statins, 3-hydroxy-3-methylglutaryl coenzyme A reductase (HMGCR), is an autoantibody target in patients that develop an immune-mediated necrotizing myopathy (IMNM). These observations have been confirmed in a number of studies but, until today, a multi-center, international study of IMNM, related idiopathic inflammatory myopathies (IIM), other auto-inflammatory conditions and controls has not been published. Accordingly, an international, multi-center study investigated the utility of anti-HMGCR antibodies in the diagnosis of statin-associated IMNM in comparison to different forms of IIM and controls. This study included samples from patients with different forms of IIM (n=1250) and patients with other diseases (n=656) that were collected from twelve sites and tested for anti-HMGCR antibodies by ELISA. This study confirmed that anti-HMGCR autoantibodies, when found in conjunction with statin use, characterize a subset of IIM who are older and have necrosis on muscle biopsy. Taken together, the data to date indicates that testing for anti-HMGCR antibodies is important in the differential diagnosis of IIM and might be considered for future classification criteria.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Auto-antibody immune complexes (ICs) mediate pathogenesis in multiple autoimmune diseases direct interference with target function, complement fixation, and interaction with Fc-gamma receptors (FcγRs). Through high avidity interactions, ICs are able to crosslink low affinity FcγRs expressed on a wide variety of effector cells, leading to secretion of pro-inflammatory mediators and inducing cytotoxicity, ultimately resulting in tissue injury. Given their relevance in numerous autoimmune diseases, FcγRs have been considered as attractive therapeutic targets for the last three decades. However, a limited number of investigational drug candidates have been developed targeting FcγRs and only a few approved therapeutics have been associated with impacting FcγRs. This review provides a historical overview of the different therapeutic approaches used to target FcγRs for the treatment of autoimmune and inflammatory diseases.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: RORγ is a nuclear hormone receptor which controls polarization of naive CD4+ T-cells into proinflammatory Th17 cells. Pharmacological antagonism of RORγ has therapeutic potential for autoimmune diseases; however, this mechanism may potentially carry target-related safety risks, as mice deficient in Rorc, the gene encoding RORγ, develop T-cell lymphoma with 50% frequency. Due to the requirement of RORγ during development, the Rorc knockout (KO) animals lack secondary lymphoid organs and have a dysregulation in the generation of CD4 + and CD8 + T cells. We wanted to extend the evaluation of RORγ deficiency to address the question whether lymphomas, similar to those observed in the Rorc KO, would develop in an animal with an otherwise intact adult immune system. Accordingly, we designed a conditional RORγ knockout mouse (Rorc CKO) where the Rorc locus could be deleted in adult animals. Based on these studies we can confirm that these animals also develop lymphoma in a similar time frame as embryonic Rorc knockouts. This study also suggests that in animals where the gene deletion is incomplete, the thymus undergoes a rapid selection process replacing Rorc deficient cells with remnant thymocytes carrying a functional Rorc locus and that subsequently, these animals do not develop lymphoblastic lymphoma.
    Article · Aug 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Diagnosis of antiphospholipid syndrome (APS) is essentially based on the detection of circulating antiphospholipid (aPL) antibodies. Progress have been made on the standardization of tests exploring the presence of aPL as guidelines on coagulation and immunological tests were recently published in the literature. Clinical relevance of aPL profile has come from prospective cohort studies in populations with a homogeneous antibody profile supporting the view that triple positivity is a high risk pattern in patients and carriers. In addition to the classic ones, several other tests have been proposed for the diagnosis of APS. The detection of antibodies directed to domain 1 and 4/5 of β2-Glycoprotein I (β2GP1) were found to be particularly sound. Several issues remain to be addressed. We do not yet know what is the physiological function of β2GP1 and the pathophysiology of thrombosis and pregnancy loss in these patients. Moreover, treatment is poorly defined especially in the case of feared catastrophic APS.
    Article · Jul 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Primary biliary cholangitis (PBC; previously "primary biliary cirrhosis") is a cholestatic, putatively autoimmune-mediated liver disease with a clear female preponderance affecting the intrahepatic small and medium-size bile ducts and resulting in bile duct destruction and ductopenia, portal fibrosis that progresses slowly to biliary cirrhosis. Despite suboptimal response in one third of patients treated with ursodeoxycholic acid (UDCA), this remains the only FDA-approved agent for this disease. In this review, we cover recent advances in research that have yielded numerous agents currently at different stages of the drug pipeline, some of which are expected to be approved in the near future. We also discuss accumulating evidence supporting the use of older agents (fibrates and glucocorticoids) as an adjunctive therapy to UDCA in non-responsive patients. We suggest that with the imminent expansion of the therapeutic armamentarium for PBC, a more comprehensive approach - ideally taking into account not only biochemical markers of disease stage - is needed to better select patients in whom these strategies might be most useful. Studies are also needed to compare the relative efficacy of different proposed second-line treatments not only against UDCA monotherapy.
    Article · Jul 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Autoimmune rheumatic diseases are chronic systemic conditions often affecting young women during their reproductive years, so that pregnancy is a major issue in their management. For a long time pregnancy has been discouraged in these women, mainly for two reasons: gestation could aggravate maternal disease and, vice versa, the disease could negatively influence the gestational outcome. The great improvement in the approach to pregnancy done in the past few decades has allowed a progressively increasing number of affected women to fulfill their family plan. Women should be informed about potential risks related to their disease, but they should also be reassured that a good pregnancy outcome is possible if conception occurs in a stable remission state, teratogenic medications have been properly withdrawn and “safe” drugs have been mantained to prevent disease flare. A brief excursus regarding the main issues regarding SLE/APS, Systemic Sclerosis and Systemic Vasculitis is provided, in the attempt to delineate the main risk factors for adverse pregnancy outcome, the onset of maternal complications and the role played by a close multi-specialistic monitoring.
    Article · Jul 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: Background: The data regarding the association between inflammatory bowel disease (IBD) and systemic lupus erythematosus (SLE) is mostly composed of case reports and case series indicating an infrequent association. Objectives: To investigate the association between IBD and SLE. Methods: Patients with SLE were compared with age- and sex-matched controls regarding the prevalence of ulcerative colitis (UC) and Crohn's disease (CD) 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. The study was performed utilizing the medical database of Clalit Health Services. Results: The study included 5018 patients with SLE and 25,090 age- and sex-matched controls. The prevalence of UC was significantly higher in patients with SLE than in controls in a univariate analysis (0.4% and 0.2%, respectively; p<0.017). However, in a multivariate logistic regression model SLE was not associated with UC (OR 1.67, 95% CI 0.99-2.815, p<0.052). The prevalence of CD was higher in patients with SLE than in controls in a univariate analysis (0.7% and 0.3%, respectively; p<0.001). A multivariate logistic regression model confirmed this finding and corroborated that SLE was associated with comorbid CD (OR 2.23, 95% CI 1.46-3.4, p<0.001). Conclusions: Patients with SLE have a greater prevalence of CD than matched controls. The distinction of IBD from SLE gastrointestinal involvement can be challenging as clinical manifestations, laboratory tests, and radiographic findings may appear similar between the two diseases. Therefore, physicians treating patients with rather IBD or SLE should consider this potential association.
    Article · Jul 2016 · Autoimmunity reviews
  • [Show abstract] [Hide abstract] ABSTRACT: The central nervous system manifestations of SLE (neuropsychiatric lupus, NPSLE) occur frequently, though are often difficult to diagnose and treat. Symptoms of NPSLE can be quite diverse, including chronic cognitive and emotional manifestations, as well as acute presentations, such as stroke and seizures. Although the pathogenesis of NPSLE has yet to be well characterized, B-cell mediated damage is believed to be an important contributor. B-cells and autoantibodies may traverse the BBB, promoting an inflammatory environment consisting of glia activation, neurodegeneration, and consequent averse behavioral outcomes. This review will evaluate the various suggested roles of B-cells and autoantibodies in NPSLE, as well as therapeutic modalities targeting these pathogenic mediators.
    Article · Jul 2016 · Autoimmunity reviews