Journal of autoimmune diseases最新文献

{"title":"Autoantibody profiles in the sera of patients with Q fever: characterization of antigens by immunofluorescence, immunoblot and sequence analysis.","authors":"M T Camacho,&nbsp;I Outschoorn,&nbsp;A Tellez,&nbsp;J Sequí","doi":"10.1186/1740-2557-2-10","DOIUrl":"https://doi.org/10.1186/1740-2557-2-10","url":null,"abstract":"<p><p>Recent reports have shown that some of the immunological aspects of Q fever, a rickettsiosis caused by Coxiella burnetii, could be related to self-antigen responses. The aim of this study was to determine the specificity of the autoantibody response of patients with acute and chronic Coxiella infections. Smooth muscle and cardiac muscle-specific autoantibodies were observed in significant percentages in acutely or chronically affected Q fever patients when compared to healthy volunteers. Moreover, the incidence of cardiac muscle-specific autoantibody was significantly higher among chronically ill patients compared to acutely ill patients. Moreover, a band of 50 kD of a HeLa extract was detected in most of the sera of individuals with chronic infections and previous sequence analysis suggests that this antigen presents a high degree of homology with the human actin elongation factor 1 alpha. Further research would be necessary to confirm if antibodies to human cytoskeletal proteins could be of clinical importance in chronically infected Q fever patients.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 ","pages":"10"},"PeriodicalIF":0.0,"publicationDate":"2005-11-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-10","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25683824","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":"Co-occurrence of autoimmune thyroid disease in a multiple sclerosis cohort.","authors":"J S Sloka,&nbsp;Pryse-W E M Phillips,&nbsp;M Stefanelli,&nbsp;C Joyce","doi":"10.1186/1740-2557-2-9","DOIUrl":"https://doi.org/10.1186/1740-2557-2-9","url":null,"abstract":"<p><strong>Background: </strong>Multiple sclerosis (MS), Hashimoto's disease and Graves' disease are autoimmune diseases that may share similar pathogenic mechanisms. The co-occurrence rates and demographic characteristics of Graves' disease and Hashimoto's disease (HT) in our MS population are compared with the general population.</p><p><strong>Methods: </strong>The prevalence of thyroid disease in our MS patients was determined by chart review and survey. Previous diagnosis of thyroid disease, age at diagnosis, treatment used, and about the use of disease modifying medications used to treat their MS were asked. Chart reviews were used to estimate the population prevalence of Graves' disease and Hashimoto's disease and to estimate the demographics of patients with thyroid disease.</p><p><strong>Results: </strong>A significant co-occurrence of Graves' disease with MS (p = 0.002), and a non-significant co-occurrence of Hashimoto's disease were noted (p = 0.097). No difference in the age of onset or gender of thyroid disease in MS patients compared to the general population was found.</p><p><strong>Conclusion: </strong>There is a significant co-occurrence in patients with MS and Graves' disease, and a trend to co-occurrence in patients with MS and Hashimoto's disease. There are no differences in the demographics of patients with thyroid disease in our MS patients compared to the general population.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 ","pages":"9"},"PeriodicalIF":0.0,"publicationDate":"2005-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-9","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25684477","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":"Lack of correlation between the levels of soluble cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and the CT-60 genotypes.","authors":"Sharad Purohit,&nbsp;Robert Podolsky,&nbsp;Christin Collins,&nbsp;Weipeng Zheng,&nbsp;Desmond Schatz,&nbsp;Andy Muir,&nbsp;Diane Hopkins,&nbsp;Yi-Hua Huang,&nbsp;Jin-Xiong She","doi":"10.1186/1740-2557-2-8","DOIUrl":"https://doi.org/10.1186/1740-2557-2-8","url":null,"abstract":"<p><strong>Background: </strong>Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) plays a critical role in downregulation of antigen-activated immune response and polymorphisms at the CTLA-4 gene have been shown to be associated with several autoimmune diseases including type-1 diabetes (T1D). The etiological mutation was mapped to the CT60-A/G single nucleotide polymorphism (SNP) that is believed to control the processing and production of soluble CTLA-4 (sCTLA-4).</p><p><strong>Methods: </strong>We therefore determined sCTLA-4 protein levels in the sera from 82 T1D patients and 19 autoantibody positive (AbP) subjects and 117 autoantibody negative (AbN) controls using ELISA. The CT-60 SNP was genotyped for these samples by using PCR and restriction enzyme digestion of a 268 bp DNA segment containing the SNP. Genotyping of CT-60 SNP was confirmed by dye terminating sequencing reaction.</p><p><strong>Results: </strong>Higher levels of sCTLA-4 were observed in T1D (2.24 ng/ml) and AbP (mean = 2.17 ng/ml) subjects compared to AbN controls (mean = 1.69 ng/ml) with the differences between these subjects becoming significant with age (p = 0.02). However, we found no correlation between sCTLA-4 levels and the CTLA-4 CT-60 SNP genotypes.</p><p><strong>Conclusion: </strong>Consistent with the higher serum sCTLA-4 levels observed in other autoimmune diseases, our results suggest that sCTLA-4 may be a risk factor for T1D. However, our results do not support the conclusion that the CT-60 SNP controls the expression of sCTLA-4.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 ","pages":"8"},"PeriodicalIF":0.0,"publicationDate":"2005-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-8","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25665291","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":"Transfer of efficient anti-melanocyte T cells from vitiligo donors to melanoma patients as a novel immunotherapeutical strategy.","authors":"Belinda Palermo, Silvia Garbelli, Stefania Mantovani, Claudia Giachino","doi":"10.1186/1740-2557-2-7","DOIUrl":"10.1186/1740-2557-2-7","url":null,"abstract":"<p><strong>Background: </strong>Vitiligo is a relatively common progressive depigmentary condition that is believed to be due to the autoimmune-mediated loss of epidermal melanocytes. High frequencies of self-reactive T lymphocytes directed toward melanocyte differentiation antigens are found in vitiligo patients and might be directly responsible for the pathogenesis of the disease. An interesting aspect of vitiligo is its relation to melanoma: cytotoxic T lymphocytes directed to self antigens shared by normal melanocytes and melanoma cells are found in both conditions, but the resulting immune reactions are completely different. From this standpoint, the selective destruction of pigment cells that occurs in cases of vitiligo is the therapeutic goal sought in melanoma research.</p><p><strong>Presentation of the hypothesis: </strong>Our working hypothesis is that vitiligo patients might represent a unique source of therapeutic cells to be used in allo-transfer for HLA-matched melanoma patients. The adoptive transfer of ex-vivo generated autologous tumor-specific T cells is a therapy that has met with only limited success, essentially because of inability to isolate therapeutically valuable T cells from the majority of tumor patients. Ideally, model systems where strong and efficient responses against the same (tumor) antigens are achieved would represent a better source of therapeutic cells. We believe it is possible to identify one such model in the melanoma-vitiligo dichotomy: T lymphocytes specific for different melanocyte differentiation antigens are found in vitiligo and represent the effective anti-melanocyte reactivity that is often ineffective in melanoma.</p><p><strong>Testing the hypothesis: </strong>Melanocyte-specific T cell clones can be isolated from the peripheral blood of vitiligo patients and tested for their capacity to efficiently expand in vitro without loosing their cytotoxic activity and to migrate to the skin. Cytotoxicity against melanoma patients' non-tumor cells can also be tested. In addition, it would be interesting to attempt an in vivo animal model. If the results obtained from these validation steps will be satisfactory, it might be possible to plan the clinical grade preparation of relevant clones for transfer.</p><p><strong>Implications of the hypothesis: </strong>When translated into a clinical trial, the possibility of in vitro selecting few effective tumor-specific T cell clones for infusion, inherent with this approach, could enhance the therapeutic graft-versus-tumor effect while possibly decreasing the risk of graft-versus-host disease.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 ","pages":"7"},"PeriodicalIF":0.0,"publicationDate":"2005-08-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1215509/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25279060","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":"Expression of TNF inhibitor gene in the lacrimal gland promotes recovery of tear production and tear stability and reduced immunopathology in rabbits with induced autoimmune dacryoadenitis.","authors":"Melvin D Trousdale,&nbsp;Zenjin Zhu,&nbsp;Douglas Stevenson,&nbsp;Joel E Schechter,&nbsp;Thomas Ritter,&nbsp;Austin K Mircheff","doi":"10.1186/1740-2557-2-6","DOIUrl":"https://doi.org/10.1186/1740-2557-2-6","url":null,"abstract":"<p><strong>Background: </strong>The most common cause of ocular morbidity in developed countries is dry eye, many cases of which are due to lacrimal insufficiency. Dry eye affects approximately 10 million in the United States, most of whom are women. In the U.S. alone, an estimated 2 million Sjögren's syndrome patients have dysfunctional lacrimal glands and severe dry eye, and there is no satisfactory treatment. These patients would benefit if their lacrimal tissue function could be restored.</p><p><strong>Methods: </strong>The effect of adenovirus-mediated transfer of tumor necrosis factor (TNF)-alpha inhibitor gene on induced autoimmune dacryoadenitis was evaluated in a rabbit model. Soluble transgene protein was detected in tears by ELISA for 7 days following transduction.</p><p><strong>Results: </strong>Two weeks after induction of disease with activated lymphocytes, tear production, as determined by Schirmer testing, was reduced by about 40%, while tear film stability, as measured by tear breakup time (BUT), declined by 43%. Adenovirus-mediated gene therapy using AdTNFRp55-Ig given 2 weeks after disease induction, resulted in the return of tear production to normal levels by week 4. In the treated disease group, tear BUT improved significantly by week 4. Rose bengal scores, an indicator of corneal surface defects, increased after disease induction and declined after gene therapy. In the lacrimal gland, the CD4 to CD8 T cell ratio was 4:1 in the disease group compared to 1:2 in the treated group. Infiltration of T cells and CD18+ cells was reduced approximately 50% after gene therapy.</p><p><strong>Conclusion: </strong>We concluded that therapeutic levels of soluble TNF inhibitor were achieved in the lacrimal gland and on the corneal surface. Anti-inflammatory cytokine gene expression might offer a potential therapeutic modality for the treatment of autoimmune dacryoadenitis, once suitable vectors become available.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 ","pages":"6"},"PeriodicalIF":0.0,"publicationDate":"2005-06-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-6","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25161631","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 autoantibodies to common and neuronal cell antigens in Chronic Fatigue Syndrome.","authors":"Suzanne D Vernon,&nbsp;William C Reeves","doi":"10.1186/1740-2557-2-5","DOIUrl":"https://doi.org/10.1186/1740-2557-2-5","url":null,"abstract":"<p><p>People with chronic fatigue syndrome (CFS) suffer from multiple symptoms including fatigue, impaired memory and concentration, unrefreshing sleep and musculoskeletal pain. The exact causes of CFS are not known, but the symptom complex resembles that of several diseases that affect the immune system and autoantibodies may provide clues to the various etiologies of CFS. We used ELISA, immunoblot and commercially available assays to test serum from subjects enrolled in a physician-based surveillance study conducted in Atlanta, Georgia and a population-based study in Wichita, Kansas for a number of common autoantibodies and antibodies to neuron specific antigens. Subsets of those with CFS had higher rates of antibodies to microtubule-associated protein 2 (MAP2) (p = 0.03) and ssDNA (p = 0.04). There was no evidence of higher rates for several common nuclear and cellular antigens in people with CFS. Autoantibodies to specific host cell antigens may be a useful approach for identifying subsets of people with CFS, identify biomarkers, and provide clues to CFS etiologies.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":" ","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2005-05-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41008873","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":"N-acetyl-L-cysteine ameliorates the inflammatory disease process in experimental autoimmune encephalomyelitis in Lewis rats.","authors":"Romesh Stanislaus,&nbsp;Anne G Gilg,&nbsp;Avtar K Singh,&nbsp;Inderjit Singh","doi":"10.1186/1740-2557-2-4","DOIUrl":"https://doi.org/10.1186/1740-2557-2-4","url":null,"abstract":"<p><p>We report that N-acetyl-L-cysteine (NAC) treatment blocked induction of TNF-alpha, IL-1beta, IFN-gamma and iNOS in the CNS and attenuated clinical disease in the myelin basic protein induced model of experimental allergic encephalomyelitis (EAE) in Lewis rats. Infiltration of mononuclear cells into the CNS and induction of inflammatory cytokines and iNOS in multiple sclerosis (MS) and EAE have been implicated in subsequent disease progression and pathogenesis. To understand the mechanism of efficacy of NAC against EAE, we examined its effect on the production of cytokines and the infiltration of inflammatory cells into the CNS. NAC treatment attenuated the transmigration of mononuclear cells thereby lessening the neuroinflammatory disease. Splenocytes from NAC-treated EAE animals showed reduced IFN-gamma production, a Th1 cytokine and increased IL-10 production, an anti-inflammatory cytokine. Further, splenocytes from NAC-treated EAE animals also showed decreased nitrite production when stimulated in vitro by LPS. These observations indicate that NAC treatment may be of therapeutic value in MS against the inflammatory disease process associated with the infiltration of activated mononuclear cells into the CNS.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 1","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2005-05-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25090210","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":"The importance of APC.","authors":"Vitaly Ablamunits","doi":"10.1186/1740-2557-2-3","DOIUrl":"https://doi.org/10.1186/1740-2557-2-3","url":null,"abstract":"<p><p>Readers in immunology are familiar with the importance of antigen presenting cells in mounting immune responses. For the purpose of this particular editorial article, however, the abbreviation APC will stand for article processing charges. The publisher will introduce APCs for this Journal in May, 2005. Here we explain why article-processing charges are important to maintain our Open Access journal.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 1","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2005-04-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25077049","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":"Localization of the immunodominant region on human thyroid peroxidase in autoimmune thyroid diseases: an update.","authors":"Damien Bresson,&nbsp;Sandra A Rebuffat,&nbsp;Sylvie Péraldi-Roux","doi":"10.1186/1740-2557-2-2","DOIUrl":"https://doi.org/10.1186/1740-2557-2-2","url":null,"abstract":"<p><p>Recent studies in the field of autoimmune thyroid diseases have largely focused on the delineation of B-cell auto-epitopes recognized by the main autoantigens to improve our understanding of how these molecules are seen by the immune system. Among these autoantigens which are targeted by autoantibodies during the development of autoimmune thyroid diseases, thyroid peroxidase is a major player. Indeed, high amounts of anti-thyroid peroxidase autoantibodies are found in the sera of patients suffering from Graves' disease and Hashimoto's thyroiditis, respectively hyper and hypothyroidism. Since anti-thyroid peroxidase autoantibodies from patients'sera mainly recognize a discontinuous immunodominant region on thyroid peroxidase and due to the complexity of the three dimensional structure of human thyroid peroxidase, numerous investigations have been necessary to closely localize this immunodominant region. The aim of the present review is to summarize the current knowledge regarding the localization of the immunodominant region recognized by human thyroid peroxidase-specific autoantibodies generated during the development of autoimmune thyroid diseases.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 1","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2005-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25006521","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":"Immunogenetics of Hashimoto's thyroiditis.","authors":"Dimitry A Chistiakov","doi":"10.1186/1740-2557-2-1","DOIUrl":"https://doi.org/10.1186/1740-2557-2-1","url":null,"abstract":"<p><p>Hashimoto's thyroiditis (HT) is an organ-specific T-cell mediated disease. It is a complex disease, with a strong genetic component. To date, significant progress has been made towards the identification and functional characterization of HT susceptibility genes. In this review, we will summarize the recent advances in our understanding of the genetic input to the pathogenesis of HT.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 1","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2005-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25170619","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}