Autoimmune Diseases最新文献_第10页

Anti-transglutaminase 6 antibodies in children and young adults with cerebral palsy. 儿童和青年脑瘫患者抗谷氨酰胺转胺酶6抗体的研究

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-04-02 DOI: 10.1155/2014/237107

Reidun Stenberg, Marios Hadjivassiliou, Pascale Aeschlimann, Nigel Hoggard, Daniel Aeschlimann

{"title":"Anti-transglutaminase 6 antibodies in children and young adults with cerebral palsy.","authors":"Reidun Stenberg, Marios Hadjivassiliou, Pascale Aeschlimann, Nigel Hoggard, Daniel Aeschlimann","doi":"10.1155/2014/237107","DOIUrl":"https://doi.org/10.1155/2014/237107","url":null,"abstract":"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. ","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}

引用次数: 11

A tandem repeat in decay accelerating factor 1 is associated with severity of murine mercury-induced autoimmunity. 衰变加速因子1串联重复序列与小鼠汞诱导的自身免疫的严重程度有关。

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-04-10 DOI: 10.1155/2014/260613

David M Cauvi, Rodney Gabriel, Dwight H Kono, Per Hultman, K Michael Pollard

{"title":"A tandem repeat in decay accelerating factor 1 is associated with severity of murine mercury-induced autoimmunity.","authors":"David M Cauvi, Rodney Gabriel, Dwight H Kono, Per Hultman, K Michael Pollard","doi":"10.1155/2014/260613","DOIUrl":"https://doi.org/10.1155/2014/260613","url":null,"abstract":"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. ","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}

引用次数: 2

Autoimmunity and asbestos exposure. 自身免疫和石棉暴露。

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-04-29 DOI: 10.1155/2014/782045

Jean C Pfau, Kinta M Serve, Curtis W Noonan

{"title":"Autoimmunity and asbestos exposure.","authors":"Jean C Pfau, Kinta M Serve, Curtis W Noonan","doi":"10.1155/2014/782045","DOIUrl":"https://doi.org/10.1155/2014/782045","url":null,"abstract":"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. ","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}

引用次数: 59

Treatment of chronic inflammatory demyelinating polyneuropathy: from molecular bases to practical considerations. 慢性炎症性脱髓鞘性多神经病变的治疗:从分子基础到实际考虑。

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-01-14 DOI: 10.1155/2014/201657

Paolo Ripellino, Thomas Fleetwood, Roberto Cantello, Cristoforo Comi

引用次数: 25

Occurrence of Autoimmune Diseases Related to the Vaccine against Yellow Fever. 与黄热病疫苗相关的自身免疫性疾病的发生

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-10-22 DOI: 10.1155/2014/473170

Ana Cristina Vanderley Oliveira, Licia Maria Henrique da Mota, Leopoldo Luiz Dos Santos-Neto, Jozélio Freire De Carvalho, Iramaya Rodrigues Caldas, Olindo Assis Martins Filho, Pedro Luis Tauil

{"title":"Occurrence of Autoimmune Diseases Related to the Vaccine against Yellow Fever.","authors":"Ana Cristina Vanderley Oliveira, Licia Maria Henrique da Mota, Leopoldo Luiz Dos Santos-Neto, Jozélio Freire De Carvalho, Iramaya Rodrigues Caldas, Olindo Assis Martins Filho, Pedro Luis Tauil","doi":"10.1155/2014/473170","DOIUrl":"https://doi.org/10.1155/2014/473170","url":null,"abstract":"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. ","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}

引用次数: 17

Evaluation of a multiplex ELISA for autoantibody profiling in patients with autoimmune connective tissue diseases. 多重ELISA检测自身免疫性结缔组织疾病患者自身抗体谱的评价

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-01-16 DOI: 10.1155/2014/896787

Alejandro Caro Pérez, Sarita Kumble, Krishnanand D Kumble, M Consuelo Alonso Cañizal, Luis M Jiménez Jiménez, Lorena Alonso Díez, Pilar Durán Parejo

{"title":"Evaluation of a multiplex ELISA for autoantibody profiling in patients with autoimmune connective tissue diseases.","authors":"Alejandro Caro Pérez, Sarita Kumble, Krishnanand D Kumble, M Consuelo Alonso Cañizal, Luis M Jiménez Jiménez, Lorena Alonso Díez, Pilar Durán Parejo","doi":"10.1155/2014/896787","DOIUrl":"https://doi.org/10.1155/2014/896787","url":null,"abstract":"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. ","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}

引用次数: 4

Evaluation of SLE Susceptibility Genes in Malaysians. 马来西亚人SLE易感基因的评估。

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-02-18 DOI: 10.1155/2014/305436

Julio E Molineros, Kek Heng Chua, Celi Sun, Lay Hoong Lian, Prasenjeet Motghare, Xana Kim-Howard, Swapan K Nath

{"title":"Evaluation of SLE Susceptibility Genes in Malaysians.","authors":"Julio E Molineros, Kek Heng Chua, Celi Sun, Lay Hoong Lian, Prasenjeet Motghare, Xana Kim-Howard, Swapan K Nath","doi":"10.1155/2014/305436","DOIUrl":"https://doi.org/10.1155/2014/305436","url":null,"abstract":"Systemic Lupus Erythematosus (SLE) is a clinically heterogeneous autoimmune disease with strong genetic and environmental components. Our objective was to replicate 25 recently identified SLE susceptibility genes in two distinct populations (Chinese (CH) and Malays (MA)) from Malaysia. We genotyped 347 SLE cases and 356 controls (CH and MA) using the ImmunoChip array and performed an admixture corrected case-control association analysis. Associated genes were grouped into five immune-related pathways. While CH were largely homogenous, MA had three ancestry components (average 82.3% Asian, 14.5% European, and 3.2% African). Ancestry proportions were significantly different between cases and controls in MA. We identified 22 genes with at least one associated SNP (P < 0.05). The strongest signal was at HLA-DRA (P Meta = 9.96 × 10(-9); P CH = 6.57 × 10(-8), P MA = 6.73 × 10(-3)); the strongest non-HLA signal occurred at STAT4 (P Meta = 1.67 × 10(-7); P CH = 2.88 × 10(-6), P MA = 2.99 × 10(-3)). Most of these genes were associated with B- and T-cell function and signaling pathways. Our exploratory study using high-density fine-mapping suggests that most of the established SLE genes are also associated in the major ethnicities of Malaysia. However, these novel SNPs showed stronger association in these Asian populations than with the SNPs reported in previous studies. ","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"305436"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/305436","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32232160","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}

引用次数: 8

Differential immunotoxicity induced by two different windows of developmental trichloroethylene exposure. 发育期接触三氯乙烯的两个不同窗口诱发的不同免疫毒性。

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-02-20 DOI: 10.1155/2014/982073

Kathleen M Gilbert, William Woodruff, Sarah J Blossom

{"title":"Differential immunotoxicity induced by two different windows of developmental trichloroethylene exposure.","authors":"Kathleen M Gilbert, William Woodruff, Sarah J Blossom","doi":"10.1155/2014/982073","DOIUrl":"10.1155/2014/982073","url":null,"abstract":"Developmental exposure to environmental toxicants may induce immune system alterations that contribute to adult stage autoimmune disease. We have shown that continuous exposure of MRL+/+ mice to trichloroethylene (TCE) from gestational day (GD) 0 to postnatal day (PND) 49 alters several aspects of CD4(+) T cell function. This window of exposure corresponds to conception-adolescence/young adulthood in humans. More narrowly defining the window of TCE developmental exposure causes immunotoxicity that would establish the stage at which avoidance and/or intervention would be most effective. The current study divided continuous TCE exposure into two separate windows, namely, gestation only (GD0 to birth (PND0)) and early-life only (PND0-PND49). The mice were examined for specific alterations in CD4(+) T cell function at PND49. One potentially long-lasting effect of developmental exposure, alterations in retrotransposon expression indicative of epigenetic alterations, was found in peripheral CD4(+) T cells from both sets of developmentally exposed mice. Interestingly, certain other effects, such as alterations in thymus cellularity, were only found in mice exposed to TCE during gestation. In contrast, expansion of memory/activation cell subset of peripheral CD4(+) T cells were only found in mice exposed to TCE during early life. Different windows of developmental TCE exposure can have different functional consequences. ","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"982073"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3950550/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32232161","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}

引用次数: 0

Silent Burdens in Disease: Fatigue and Depression in SLE. 疾病中的隐性负担:SLE患者的疲劳和抑郁。

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-01-28 DOI: 10.1155/2014/790724

R Fonseca, M Bernardes, G Terroso, M de Sousa, M Figueiredo-Braga

{"title":"Silent Burdens in Disease: Fatigue and Depression in SLE.","authors":"R Fonseca, M Bernardes, G Terroso, M de Sousa, M Figueiredo-Braga","doi":"10.1155/2014/790724","DOIUrl":"https://doi.org/10.1155/2014/790724","url":null,"abstract":"At a time when health is being recognized as more than just avoiding death, age and comorbidity are becoming increasingly important aspects of chronic disease. Systemic Lupus Erythematous (SLE) is probably one of the best paradigms of modern chronic disease, sitting at the crossroads of numerous somatic health problems, immune activation, depression, pain, and fatigue. One hundred forty-eight female participants were enrolled in the present study: 50 diagnosed with SLE, 45 with major depressive disorder (MDD), and 53 age-matched controls. Statistically significant lower scores in quality-of-life dimensions related to physical impairment were found in SLE. Patients with MDD presented significant levels of pain, reduced physical summary component (PSC), and general health scores different from healthy controls. Fatigue was reported in 90% of women with SLE and 77.8% of the MDD patients in contrast with 39.6% in the control group. Significant correlations were seen among fatigue severity, age, and educational level in SLE. From our own previous work and more recent work on the association of immune activation and depression, unexplained fatigue in SLE may signify an early sign of immune activation flare-up. The search for cytokine markers should perhaps be extended to fatigue in SLE. ","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"790724"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/790724","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32174770","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}

引用次数: 44

Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease? 适应性免疫在年龄相关性黄斑变性中的潜在来源和作用:我们是否应该将AMD重新命名为自身免疫性黄斑疾病?

IF 4

Autoimmune Diseases Pub Date : 2014-01-01 Epub Date: 2014-04-30 DOI: 10.1155/2014/532487

Serge Camelo

{"title":"Potential Sources and Roles of Adaptive Immunity in Age-Related Macular Degeneration: Shall We Rename AMD into Autoimmune Macular Disease?","authors":"Serge Camelo","doi":"10.1155/2014/532487","DOIUrl":"https://doi.org/10.1155/2014/532487","url":null,"abstract":"Age-related macular degeneration (AMD) is the leading cause of vision loss in the elderly throughout the industrialized world. Its most prominent pathologic features are lesions involving the retinal pigment epithelium (RPE) the Bruch's membrane, the degeneration of photoreceptors, and, in the most aggressive cases, choroidal neovascularization. Genetic associations between the risk of developing AMD and polymorphism within components of the complement system, as well as chemokine receptors expressed on microglial cells and macrophages, have linked retinal degeneration and choroidal neovascularization to innate immunity (inflammation). In addition to inflammation, players of the adaptive immunity including cytokines, chemokines, antibodies, and T cells have been detected in animal models of AMD and in patients suffering from this pathology. These observations suggest that adaptive immunity might play a role in different processes associated with AMD such as RPE atrophy, neovascularization, and retinal degeneration. To this date however, the exact roles (if any) of autoantibodies and T cells in AMD remain unknown. In this review we discuss the potential effects of adaptive immune responses in AMD pathogenesis. ","PeriodicalId":46314,"journal":{"name":"Autoimmune Diseases","volume":"2014 ","pages":"532487"},"PeriodicalIF":4.0,"publicationDate":"2014-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1155/2014/532487","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32379779","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}

引用次数: 57