Autoimmune Diseases最新文献

{"title":"Environmental triggers and autoimmunity.","authors":"Aristo Vojdani, K Michael Pollard, Andrew W Campbell","doi":"10.1155/2014/798029","DOIUrl":"https://doi.org/10.1155/2014/798029","url":null,"abstract":"Currently, studies have shown that genetic predisposition accounts for approximately thirty percent of all autoimmune diseases. The rest, 70 percent, are due to environmental factors, including toxic chemicals, dietary components, gut dysbiosis, and infections (Figure 1). \u0000 \u0000 \u0000 \u0000Figure 1 \u0000 \u0000Factors that contribute to autoimmune disease. \u0000 \u0000 \u0000 \u0000Autoimmune disorder symptoms are initially nonspecific and include malaise and fatigue, low-grade fevers, aches, and pains. Due to this vagueness, patients are frequently diagnosed with an autoimmune disease after they become weak and unable to function normally, making the onset of the disease difficult to pinpoint and the possible triggers uncertain. \u0000 \u0000In this issue, we present a series of papers that review, discuss, and elaborate on various environmental triggers of autoimmunity. \u0000 \u0000A. Vojdani presents an extensive review of potential triggers of autoimmunity. The author discusses the loss of immune homeostasis and explains the mechanism of autoimmunity as related to infectious triggers by molecular mimicry, epitope spreading, and bystander activation. He describes the effects of dietary components, focusing particularly on recent studies with sodium chloride to explain the effects of this commonly used mineral on the immune system, in particular TH17, leading to an increased risk of autoimmunity. Milk and wheat components are reviewed, as are gluten sensitivity, celiac disease, and oral pathogens in their role in the induction of autoimmune diseases. \u0000 \u0000Over the last few years, studies have amplified our previous knowledge of the gut and demonstrated its wide-ranging importance and its potentials for triggering autoimmunity when dysbiosis occurs as a result of environmental factors (Figure 2). A. W. Campbell's review brings up essential facts about some of these environmental factors affecting not only the gut but also the mucosal immunity and describes gut microbiota links to autoimmune diseases. The author discusses the importance of early detection of autoimmunity via antibody testing to bring about a better outcome for patients by removing offending triggers. \u0000 \u0000 \u0000 \u0000Figure 2 \u0000 \u0000Mechanism for the induction of autoimmunity and neuroautoimmunity by environmental triggers. \u0000 \u0000 \u0000 \u0000A very interesting research article is presented in this issue by I. Burazor and A. Vojdani, discussing the strong link between poor dental health and cardiovascular disease due to several bacteria and then studying the potential association between these pathogens, the antibodies produced against them, and elevation of markers for inflammation in patients with acute myocardial atherothrombosis (AMA). \u0000 \u0000Decay-accelerating factor 1 (DAF1) or CD55 is a 70 KDa member of proteins which regulates complement system on the cell surfaces and protects cells from complement attack. In their review, C. B. Toomey et al. discussed the relationship between DAF1 and the complement system in the regulation of environmentally induced autoimm","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"798029"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/798029","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"33323622","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Serum leptin levels in treatment-naive patients with clinically isolated syndrome or relapsing-remitting multiple sclerosis.","authors":"Maria Eleftheria Evangelopoulos,&nbsp;Georgios Koutsis,&nbsp;Manolis Markianos","doi":"10.1155/2014/486282","DOIUrl":"https://doi.org/10.1155/2014/486282","url":null,"abstract":"<p><p>Several studies have investigated leptin levels in patients with multiple sclerosis (MS) with somewhat conflicting results. They have all focused on patients with established relapsing-remitting (RR) MS but have not specifically looked at patients with clinically isolated syndrome (CIS) suggestive of MS, in the early stages of disease. In this study, serum leptin levels were measured in 89 treatment-naïve patients with CIS (53 patients) or RRMS (36 patients) and 73 controls searching for differences between the groups and for associations with several disease parameters. The expected significant sexual dimorphism in leptin levels (higher levels in females) was observed in both MS patients and controls. Increased leptin levels were found in female patients with RRMS compared to female controls (P = .003) and female CIS patients (P = .001). Female CIS patients had comparable levels to controls. Leptin levels correlated positively to disease duration, but not to EDSS, in female patients with RRMS. The results of the present study do not indicate involvement of leptin in the early stages of MS. Normal leptin levels in patients with CIS suggest that leptin does not have a pathogenic role. The ratio leptin/BMI increases during disease course in female MS patients in a time-dependent and disability-independent manner. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"486282"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/486282","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32908882","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current understanding on the role of standard and immunoproteasomes in inflammatory/immunological pathways of multiple sclerosis.","authors":"Elena Bellavista,&nbsp;Aurelia Santoro,&nbsp;Daniela Galimberti,&nbsp;Cristoforo Comi,&nbsp;Fabio Luciani,&nbsp;Michele Mishto","doi":"10.1155/2014/739705","DOIUrl":"https://doi.org/10.1155/2014/739705","url":null,"abstract":"<p><p>The ubiquitin-proteasome system is the major intracellular molecular machinery for protein degradation and maintenance of protein homeostasis in most human cells. As ubiquitin-proteasome system plays a critical role in the regulation of the immune system, it might also influence the development and progression of multiple sclerosis (MS). Both ex vivo analyses and animal models suggest that activity and composition of ubiquitin-proteasome system are altered in MS. Proteasome isoforms endowed of immunosubunits may affect the functionality of different cell types such as CD8(+) and CD4(+) T cells and B cells as well as neurons during MS development. Furthermore, the study of proteasome-related biomarkers, such as proteasome antibodies and circulating proteasomes, may represent a field of interest in MS. Proteasome inhibitors are already used as treatment for cancer and the recent development of inhibitors selective for immunoproteasome subunits may soon represent novel therapeutic approaches to the different forms of MS. In this review we describe the current knowledge on the potential role of proteasomes in MS and discuss the pro et contra of possible therapies for MS targeting proteasome isoforms. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"739705"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/739705","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32112645","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Potential Link between Environmental Triggers and Autoimmunity.","authors":"Aristo Vojdani","doi":"10.1155/2014/437231","DOIUrl":"10.1155/2014/437231","url":null,"abstract":"<p><p>Autoimmune diseases have registered an alarming rise worldwide in recent years. Accumulated evidence indicates that the immune system's ability to distinguish self from nonself is negatively impacted by genetic factors and environmental triggers. Genetics is certainly a factor, but since it normally takes a very long time for the human genetic pattern to change enough to register on a worldwide scale, increasingly the attention of studies has been focused on the environmental factors of a rapidly changing and evolving civilization. New technology, new industries, new inventions, new chemicals and drugs, and new foods and diets are constantly and rapidly being introduced in this fast-paced ever-changing world. Toxicants, infections, epitope spreading, dysfunctions of immune homeostasis, and dietary components can all have an impact on the body's delicate immune recognition system. Although the precise etiology and pathogenesis of many autoimmune diseases are still unknown, it would appear from the collated studies that there are common mechanisms in the immunopathogenesis of multiple autoimmune reactivities. Of particular interest is the citrullination of host proteins and their conversion to autoantigens by the aforementioned environmental triggers. The identification of these specific triggers of autoimmune reactivity is essential then for the development of new therapies for autoimmune diseases. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"437231"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3945069/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32225529","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anti-transglutaminase 6 antibodies in children and young adults with cerebral palsy.","authors":"Reidun Stenberg,&nbsp;Marios Hadjivassiliou,&nbsp;Pascale Aeschlimann,&nbsp;Nigel Hoggard,&nbsp;Daniel Aeschlimann","doi":"10.1155/2014/237107","DOIUrl":"https://doi.org/10.1155/2014/237107","url":null,"abstract":"<p><p>Objectives. We have previously reported a high prevalence of gluten-related serological markers (GRSM) in children and young adults with cerebral palsy (CP). The majority had no enteropathy to suggest coeliac disease (CD). Antibodies against transglutaminase 6 (anti-TG6) represent a new marker associated with gluten-related neurological dysfunction. The aim of this study was to investigate the prevalence of anti-TG6 antibodies in this group of individuals with an early neurological injury resulting in CP. Materials and Methods. Sera from 96 patients with CP and 36 controls were analysed for IgA/IgG class anti-TG6 by ELISA. Results. Anti-TG6 antibodies were found in 12/96 (13%) of patients with CP compared to 2/36 (6%) in controls. The tetraplegic subgroup of CP had a significantly higher prevalence of anti-TG6 antibodies 6/17 (35%) compared to the other subgroups and controls. There was no correlation of anti-TG6 autoantibodies with seropositivity to food proteins including gliadin. Conclusions. An early brain insult and associated inflammation may predispose to future development of TG6 autoimmunity. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"237107"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/237107","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32322661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A tandem repeat in decay accelerating factor 1 is associated with severity of murine mercury-induced autoimmunity.","authors":"David M Cauvi,&nbsp;Rodney Gabriel,&nbsp;Dwight H Kono,&nbsp;Per Hultman,&nbsp;K Michael Pollard","doi":"10.1155/2014/260613","DOIUrl":"https://doi.org/10.1155/2014/260613","url":null,"abstract":"<p><p>Decay accelerating factor (DAF), a complement-regulatory protein, protects cells from bystander complement-mediated lysis and negatively regulates T cells. Reduced expression of DAF occurs in several systemic autoimmune diseases including systemic lupus erythematosus, and DAF deficiency exacerbates disease in several autoimmune models, including murine mercury-induced autoimmunity (mHgIA). Daf1, located within Hmr1, a chromosome 1 locus associated in DBA/2 mice with resistance to mHgIA, could be a candidate. Here we show that reduced Daf1 transcription in lupus-prone mice was not associated with a reduction in the Daf1 transcription factor SP1. Studies of NZB mice congenic for the mHgIA-resistant DBA/2 Hmr1 locus suggested that Daf1 expression was controlled by the host genome and not the Hmr1 locus. A unique pentanucleotide repeat variant in the second intron of Daf1 in DBA/2 mice was identified and shown in F2 intercrosses to be associated with less severe disease; however, analysis of Hmr1 congenics indicated that this most likely reflected the presence of autoimmunity-predisposing genetic variants within the Hmr1 locus or that Daf1 expression is mediated by the tandem repeat in epistasis with other genetic variants present in autoimmune-prone mice. These studies argue that the effect of DAF on autoimmunity is complex and may require multiple genetic elements. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"260613"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/260613","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32333196","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmunity and asbestos exposure.","authors":"Jean C Pfau,&nbsp;Kinta M Serve,&nbsp;Curtis W Noonan","doi":"10.1155/2014/782045","DOIUrl":"https://doi.org/10.1155/2014/782045","url":null,"abstract":"<p><p>Despite a body of evidence supporting an association between asbestos exposure and autoantibodies indicative of systemic autoimmunity, such as antinuclear antibodies (ANA), a strong epidemiological link has never been made to specific autoimmune diseases. This is in contrast with another silicate dust, crystalline silica, for which there is considerable evidence linking exposure to diseases such as systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis. Instead, the asbestos literature is heavily focused on cancer, including mesothelioma and pulmonary carcinoma. Possible contributing factors to the absence of a stronger epidemiological association between asbestos and autoimmune disease include (a) a lack of statistical power due to relatively small or diffuse exposure cohorts, (b) exposure misclassification, (c) latency of clinical disease, (d) mild or subclinical entities that remain undetected or masked by other pathologies, or (e) effects that are specific to certain fiber types, so that analyses on mixed exposures do not reach statistical significance. This review summarizes epidemiological, animal model, and in vitro data related to asbestos exposures and autoimmunity. These combined data help build toward a better understanding of the fiber-associated factors contributing to immune dysfunction that may raise the risk of autoimmunity and the possible contribution to asbestos-related pulmonary disease. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"782045"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/782045","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32379780","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Treatment of chronic inflammatory demyelinating polyneuropathy: from molecular bases to practical considerations.","authors":"Paolo Ripellino,&nbsp;Thomas Fleetwood,&nbsp;Roberto Cantello,&nbsp;Cristoforo Comi","doi":"10.1155/2014/201657","DOIUrl":"https://doi.org/10.1155/2014/201657","url":null,"abstract":"<p><p>Chronic inflammatory demyelinating polyneuropathy (CIDP) is an autoimmune disease of the peripheral nervous system, in which both cellular and humoral immune responses are involved. The disease is clinically heterogeneous with some patients displaying pure motor form and others also showing a variable degree of sensory dysfunction; disease evolution may also differ from patient to patient, since monophasic, progressive, and relapsing forms are reported. Underlying such clinical variability there is probably a broad spectrum of molecular dysfunctions that are and will be the target of therapeutic strategies. In this review we first explore the biological bases of current treatments and subsequently we focus on the practical management that must also take into account pharmacoeconomic issues. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"201657"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/201657","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32115304","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Occurrence of Autoimmune Diseases Related to the Vaccine against Yellow Fever.","authors":"Ana Cristina Vanderley Oliveira,&nbsp;Licia Maria Henrique da Mota,&nbsp;Leopoldo Luiz Dos Santos-Neto,&nbsp;Jozélio Freire De Carvalho,&nbsp;Iramaya Rodrigues Caldas,&nbsp;Olindo Assis Martins Filho,&nbsp;Pedro Luis Tauil","doi":"10.1155/2014/473170","DOIUrl":"https://doi.org/10.1155/2014/473170","url":null,"abstract":"<p><p>Yellow fever is an infectious disease, endemic in South America and Africa. This is a potentially serious illness, with lethality between 5 and 40% of cases. The most effective preventive vaccine is constituted by the attenuated virus strain 17D, developed in 1937. It is considered safe and effective, conferring protection in more than 90% in 10 years. Adverse effects are known as mild reactions (allergies, transaminases transient elevation, fever, headache) and severe (visceral and neurotropic disease related to vaccine). However, little is known about its potential to induce autoimmune responses. This systematic review aims to identify the occurrence of autoinflammatory diseases related to 17D vaccine administration. Six studies were identified describing 13 possible cases. The diseases were Guillain-Barré syndrome, multiple sclerosis, multiple points evanescent syndrome, acute disseminated encephalomyelitis, autoimmune hepatitis, and Kawasaki disease. The data suggest that 17D vaccination may play a role in the mechanism of loss of self-tolerance. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"473170"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/473170","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32822070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluation of a multiplex ELISA for autoantibody profiling in patients with autoimmune connective tissue diseases.","authors":"Alejandro Caro Pérez,&nbsp;Sarita Kumble,&nbsp;Krishnanand D Kumble,&nbsp;M Consuelo Alonso Cañizal,&nbsp;Luis M Jiménez Jiménez,&nbsp;Lorena Alonso Díez,&nbsp;Pilar Durán Parejo","doi":"10.1155/2014/896787","DOIUrl":"https://doi.org/10.1155/2014/896787","url":null,"abstract":"<p><p>The performance of immunoassays for the detection of autoantibodies is of critical importance in the diagnosis and assessment of patients with autoimmune connective tissue diseases (ACTD). Our objective was to compare the features of two multiplexed assays-INNO-LIA ANA and Gennova-PictArray ENA ELISA-for measurement of multiple autoantibodies and their utility as a clinical tool in ACTD diagnosis. The antigens included SS-A/Ro (60 and 52), SSB/La, Sm, Sm/RNP, CENP-B, Jo-1, and Scl-70. Stored sera from 85 ACTD patients and 80 controls consisting of patients with vasculitis, rheumatoid arthritis and infectious diseases, as well as healthy subjects were analyzed jointly with clinical and laboratory data. Agreement between the two methods varied between 58 and 99% (Cohen's kappa: 0.21-0.71) mostly for SSA and SSB. The frequency of specific autoantibodies measured using the two methods was more variable for SSA, SSB, and RNP/Sm. There were a higher number of ambiguous results when using INNO-LIA. The optimized cut-off values of the Gennova-PictArray resulted in over 99% specificities in samples obtained from the control group. Sensitivity patterns were more accurate in Gennova-PictArray than in INNO-LIA, as suggested in previously reported studies. A third method could be applied to determine which of the two methods is more accurate. </p>","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"896787"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/896787","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32115382","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}