Journal of autoimmune diseases最新文献

{"title":"Islet cell autoantibodies in African patients with Type 1 and Type 2 diabetes in Dar es Salaam Tanzania: a cross sectional study.","authors":"J J K Lutale,&nbsp;H Thordarson,&nbsp;P I Holm,&nbsp;G E Eide,&nbsp;K Vetvik","doi":"10.1186/1740-2557-4-4","DOIUrl":"https://doi.org/10.1186/1740-2557-4-4","url":null,"abstract":"<p><strong>Background: </strong>The aim of the present study was to assess the occurrence of glutamic acid decarboxylase autoantibodies (GADA) and insulinoma antigen 2 autoantibodies (IA2A) among patients of African origin in Dar es Salaam, Tanzania and to compare the occurrence of autoimmune mediated Type 1 diabetes with findings previously reported from the same place and from other African diabetic populations.</p><p><strong>Methods: </strong>Two hundred and forty five patients from the diabetic clinic at Muhimbili Hospital were recruited for a cross sectional study. Patients were clinically classified into groups with Type 1 (T1D) and Type 2 diabetes (T2D); there were 94 patients with T1D and 151 with T2D. Autoantibodies for GAD and IA2 were measured with an assay based on radioligand binding. Fasting and random blood glucose, HbA1c, and C-peptide levels were also determined.</p><p><strong>Results: </strong>Of the patients with T1D, 28 (29.8%) were GADA positive and 20 (21.3%) were IA2A positive. The overall occurrence of any autoantibody was 42.6%. The GAD and IA2 autoantibodies were detected more frequently among patients with T1D than among patients with T2D (P < 0.001). A higher autoantibody prevalence was observed with combined GADA and IA2A measurements compared to individual autoantibody measurements; 40 (42.6%) patients with T1D versus 11 (7.3%) with T2D had at least one positive autoantibody titer. There was no correlation between duration of disease and detection of autoantibodies in patients with T1D. There was a strong association with family history of diabetes among the autoantibody positive versus autoantibody negative patients with T1D (p < 0.01).</p><p><strong>Conclusion: </strong>The prevalence of GAD and IA2 autoantibodies among African patients with T1D in Dar es Salaam was the same as that reported previously for South Africa and Ethiopia. It was much higher than the prevalence of islet cell autoantibodies (ICA) reported from the same clinic about 15 years ago. For unknown reasons the prevalence of pancreatic related autoantibodies in this African population is lower than the prevalence found among Caucasian populations.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"4 ","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2007-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-4-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27069742","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 revised international autoimmune hepatitis score in chronic liver diseases including autoimmune hepatitis/overlap syndromes and autoimmune hepatitis with concurrent other liver disorders.","authors":"Panagiotis A Papamichalis, Kalliopi Zachou, George K Koukoulis, Aikaterini Veloni, Efthimia G Karacosta, Lampros Kypri, Ioannis Mamaloudis, Stella Gabeta, Eirini I Rigopoulou, Ansgar W Lohse, George N Dalekos","doi":"10.1186/1740-2557-4-3","DOIUrl":"10.1186/1740-2557-4-3","url":null,"abstract":"<p><strong>Background: </strong>We conducted a study in order to determine the usefulness and diagnostic value of International Autoimmune Hepatitis Group (IAHG) score in non-autoimmune hepatitis (AIH) hepatic disorders as well as in AIH/overlap syndromes and in cases with coexistence of AIH and other liver diseases.</p><p><strong>Methods: </strong>We applied the IAHG score in 423 patients with liver diseases excluding patients with AIH, AIH/overlap syndromes and AIH with concurrent other liver disease namely, patients with chronic hepatitis B (n = 109), chronic hepatitis C (n = 95), chronic hepatitis D (n = 4), alchoholic liver disease (n = 28), non-alcoholic fatty liver disease (n = 55), autoimmune cholestatic liver diseases (n = 77), liver disorders of undefined origin (n = 32) and with miscellaneous hepatic disorders (n = 23). 24 patients with AIH associated with any kind of liver disorder including 10 patients with AIH/overlap syndromes and 14 AIH with concurrent other liver disease were also investigated. 43 patients with AIH consisted the control group.</p><p><strong>Results: </strong>The specificity of the score was 98.1% while the sensitivity in unmasking AIH in patients with either AIH/overlap syndromes or AIH with concurrent other liver diseases was only 50% and 78.6%. In the binary logistic regression model, the presence of other autoimmune diseases (p < 0.001), the total histological score (p < 0.001) and positivity for autoantibodies (p < 0.05) were identified as independent predictors for the presnce of AIH/ovea syndromes o AI with concurren other liver diseass.</p><p><strong>Conclusion: </strong>The IAHG scoring system has very good specificity for excluding AIH in patients with chronic liver diseases but not that sensitivity in order to unmask AIH/overlap syndromes or AIH with concurrent other liver diseases. The presence of other autoimmune diseases or autoantibody markers in the absence of hepatitis viral markers should alarm physicians for the possible presence of AIH either as \"pure\" AIH or in association with other liver disorders (AIH/overlap syndromes or AIH with concurrent other liver diseases). Under these conditions, liver histology seems essential and it must always be included in the work up of hepatic patients.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"4 ","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2007-06-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1933536/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26808079","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":"Autoimmune hepatitis-specific antibodies against soluble liver antigen and liver cytosol type 1 in patients with chronic viral hepatitis.","authors":"Eirini I Rigopoulou, Maria Mytilinaiou, Ourania Romanidou, Christos Liaskos, George N Dalekos","doi":"10.1186/1740-2557-4-2","DOIUrl":"10.1186/1740-2557-4-2","url":null,"abstract":"<p><strong>Background: </strong>Non-organ specific autoantibodies are highly prevalent in patients with chronic hepatitis C (HCV). Among them, anti-liver kidney microsomal type 1 (LKM1) antibody--the serological marker of type 2 autoimmune hepatitis (AIH-2)--is detected in up to 11% of the HCV-infected subjects. On the other hand, anti-liver cytosol type 1 antibodies (anti-LC1)--either in association with anti-LKM1, or in isolation--and anti-soluble liver antigen antibodies (anti-SLA) have been considered as useful and specific diagnostic markers for AIH. However, their specificity for AIH has been questioned by some recent studies, which have shown the detection of anti-LC1 and anti-SLA by immunoprecipitation assays in HCV patients irrespective of their anti-LKM1 status. The aim of the present study was to test the anti-LC1 and anti-SLA presence by specific enzyme linked immunosorbent assays (ELISAs), in a large group of Greek HCV-infected patients with or without anti-LKM1 reactivity as firstly, immunoprecipitation assays are limited to few specialized laboratories worldwide and cannot be used routinely and secondly, to assess whether application of such tests has any relevance in the context of patients with viral hepatitis since antibody detection based on such ELISAs has not been described in detail in large groups of HCV patients.</p><p><strong>Methods: </strong>One hundred and thirty eight consecutive HCV patients (120 anti-LKM1 negative and 18 anti-LKM1 positive) were investigated for the presence of anti-LC1 and anti-SLA by commercial ELISAs. A similar number (120) of chronic hepatitis B virus (HBV) infected patients seronegative for anti-LKM1 was also tested as pathological controls.</p><p><strong>Results: </strong>Six out of 18 (33%) anti-LKM(pos)/HCV(pos) patients tested positive for anti-LC1 compared to 1/120 (0.83%) anti-LKM(neg)/HCV(pos) patients and 0/120 (0%) of the anti-LKM1(neg)/HBV(pos) patients (p < 0.001 for both comparisons). Anti-SLA antibodies were not present in any of the HCV (with or without anti-LKM1) or HBV-infected patients.</p><p><strong>Conclusion: </strong>We showed that anti-LC1 and anti-SLA autoantibodies are not detected by conventional assays in a large group of anti-LKM1 negative patients with chronic hepatitis B and C infections. Based on these results we cannot find any justification for the application of anti-LC1 and anti-SLA tests in the routine laboratory testing of viral hepatitis-related autoantibody serology with the only potential exception being the anti-LC1 screening in anti-LKM1(pos)/HCV(pos) patients.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"4 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2007-02-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1796878/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26531377","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":"Autoantibodies against the chromosomal passenger protein INCENP found in a patient with Graham Little-Piccardi-Lassueur syndrome.","authors":"Beatriz Rodríguez-Bayona,&nbsp;Sandrine Ruchaud,&nbsp;Carmen Rodríguez,&nbsp;Mario Linares,&nbsp;Antonio Astola,&nbsp;Manuela Ortiz,&nbsp;William C Earnshaw,&nbsp;Manuel M Valdivia","doi":"10.1186/1740-2557-4-1","DOIUrl":"https://doi.org/10.1186/1740-2557-4-1","url":null,"abstract":"<p><strong>Background: </strong>Graham Little - Piccardi - Lassueur (GLPL) syndrome is a rare dermatosis characterized by scarring alopecia, loss of pubic and axillary hair, and progressive development of variously located follicular papules. We report a first case ever of an autoimmune response in a patient suffering from GLPL syndrome.</p><p><strong>Methods: </strong>Immunofluorescence and immunoblot analysis were used in a variety of cell cultures including human, monkey, hamster, mouse and bovine cells to analyze the presence of autoantibodies in a GLPL patient.</p><p><strong>Results: </strong>The autoimmune serum showed a pattern of centromere and spindle microtubule staining resembling that of the chromosomal passenger protein complex. By using a complex of proteins expressed in baculovirus, immunoblot analysis demonstrated that the INCENP protein is a major autoantigen in this patient with GLPL syndrome.</p><p><strong>Conclusion: </strong>An autoimmune response in GLPL syndrome is reported against the INCENP centromere protein. The occasional development of autoimmunity in GLPL patients could serve as a test in continuing efforts to detect this disease and for a more directed therapy based on the autoantigen response.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"4 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2007-01-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-4-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26489079","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":"Decreased levels of metalloproteinase-9 and angiogenic factors in skin lesions of patients with psoriatic arthritis after therapy with anti-TNF-alpha.","authors":"Paola Cordiali-Fei,&nbsp;Elisabetta Trento,&nbsp;Giovanna D'Agosto,&nbsp;Valentina Bordignon,&nbsp;Anna Mussi,&nbsp;Marco Ardigò,&nbsp;Antonio Mastroianni,&nbsp;Antonella Vento,&nbsp;Francesco Solivetti,&nbsp;Enzo Berardesca,&nbsp;Fabrizio Ensoli","doi":"10.1186/1740-2557-3-5","DOIUrl":"https://doi.org/10.1186/1740-2557-3-5","url":null,"abstract":"<p><strong>Background: </strong>Inflammation represents an early and key event in the development of both the cutaneous psoriasis and psoriatic arthritis. Compelling evidences indicate that the production of TNF-alpha plays a central role in psoriasis by sustaining the inflammatory process in the skin as well as in the joints. Among the multiple effects produced by TNF-alpha on keratinocytes, the induction of matrix metalloproteinase-9 (MMP-9), a collagenase implicated in joint inflammatory arthritis which acts as an angiogenesis promoting factor, might represent a key mechanism in the pathogenesis of the disease. Aims of the present study were to investigate a) the role of MMP-9 in the development of psoriasis by assessing the presence of MMP-9 in lesional skin and in sera of psoriatic patients; b) the association of MMP-9 with the activity of the disease; c) the relationship between MMP-9 and TNF-alpha production.</p><p><strong>Methods: </strong>Eleven psoriatic patients, clinically presenting joint symptoms associated to the cutaneous disease, were included in a therapeutic protocol based on the administration of anti-TNF-alpha monoclonal antibody (Infliximab). Sera and skin biopsies were collected before treatment and after 6 weeks of therapy. Tissues were kept in short term cultures and production soluble mediators such as TNF-alpha, MMP-9, MMP-2, VEGF and E-Selectin, which include angiogenic molecules associated to the development of plaque psoriasis, were measured in the culture supernatants by immunoenzymatic assays (ng/ml or pg/ml per mg of tissue). MMP-9 concentrations were also measured in the sera. The cutaneous activity of disease was evaluated by the Psoriasis Area and Severity Index (PASI).</p><p><strong>Results: </strong>Clinical and laboratory assessment indicated that all but one patients had a significant improvement of the PASI score after three months of therapy. The clinical amelioration was associated to a significant decrease of MMP-9 (P = 0.017), TNF-alpha (P = 0.005) and E-selectin (P = 0.018) levels, spontaneously released by lesional biopsies before and after therapy. In addition, significant correlations were found between the PASI measurements and TNF-alpha (r2 = 0.33, P = 0.005), MMP-9 (r2 = 0.25, P = 0.017), E-selectin (r2 = 0.24, P = 0.018) production. MMP-9 levels were significantly correlated with those of TNF-alpha (r2 = 0.30, P = 0.008). A significant decrease of MMP-9 in the sera, associated to the clinical improvement was also found.</p><p><strong>Conclusion: </strong>Our findings show the existence of a direct relationship between MMP-9 and TNF-alpha production strongly suggesting that MMP-9 may play a key role in the skin inflammatory process in psoriasis.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"3 ","pages":"5"},"PeriodicalIF":0.0,"publicationDate":"2006-10-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-3-5","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26294182","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 antibodies against human HSP60 in patients with MPO-ANCA associated glomerulonephritis: a cohort study.","authors":"Marjan C Slot,&nbsp;Ruud Theunissen,&nbsp;Pieter van Paassen,&nbsp;Jan G M C Damoiseaux,&nbsp;Jan Willem Cohen Tervaert","doi":"10.1186/1740-2557-3-4","DOIUrl":"https://doi.org/10.1186/1740-2557-3-4","url":null,"abstract":"<p><strong>Background: </strong>Human Heat Shock Protein 60 (hHSP60) has been implicated in autoimmunity through molecular mimicry, based on the high degree of homology with HSP65 of micro-organisms leading to autoimmune recognition of the human protein. Additionally, sequence homology between hHSP60 and myeloperoxidase (MPO) has been described. MPO is a major autoantigen in vasculitis associated with antineutrophil cytoplasmic antibodies (ANCA). We hypothesized that infections may trigger the ANCA response against MPO through hHSP60.</p><p><strong>Methods: </strong>In 86 consecutive patients with ANCA-associated vasculitis (AAV), anti-hHSP60 and anti-mycobacterial HSP65 were measured by ELISA. Patients were compared with 69 healthy controls (HC). Continuous data between groups were compared using Wilcoxon signed rank test and Kruskal-Wallis test with Dunn's post-test when appropriate. Correlations between data were derived using Spearman correlation. Odds ratios and 95% confidence intervals were obtained using Fisher's exact test.</p><p><strong>Results: </strong>At diagnosis, median anti-mHSP65 level was higher in AAV (median [range]: 42.5 [0-500]), and subsequently in MPO-ANCA (44 [7-500]), compared to HC (22 [0-430]). Anti-hHSP60 levels in AAV were not higher compared to HC (18 [0-319] and 18.5 [0-98], respectively). However, in MPO-ANCA anti-hHSP60 levels were increased (32.5 [0-319]) compared to PR3-ANCA (13 [0-79]) and HC. We could not detect cross-reactivity between hHSP60 and MPO-ANCA. There was a correlation between anti-mHSP65 and anti-hHSP60 levels (r = 0.32, P = 0.003) but not between anti-hHSP60 and MPO-ANCA (r = -0.064, P = 0.69).</p><p><strong>Conclusion: </strong>Antibodies against mHSP65 are higher in AAV compared to HC, and anti-hHSP60 antibodies are higher in patients with MPO-ANCA than in patients with PR3-ANCA and HC. Although this finding may be indicative for cross-reactivity between MPO-ANCA and hHSP60, additional assays did not support this hypothesis.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"3 ","pages":"4"},"PeriodicalIF":0.0,"publicationDate":"2006-05-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-3-4","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26399403","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":"Cerebrovascular disease associated with antiphospholipid antibodies: more questions than answers.","authors":"Carolyn Hawkins,&nbsp;Paul Gatenby,&nbsp;Roger Tuck,&nbsp;Gytis Danta,&nbsp;Colin Andrews","doi":"10.1186/1740-2557-3-3","DOIUrl":"https://doi.org/10.1186/1740-2557-3-3","url":null,"abstract":"<p><p>Neurological syndromes occur in a significant number of patients with antiphospholipid antibodies. The optimal management for these patients however remains uncertain. Our study is a descriptive analysis looking retrospectively at 45 patients who presented to the principal tertiary referral centre in the Australian Capital Territory, with either cerebral arterial or venous thrombosis for which there was no obvious cause for their presentation when initially reviewed. The diagnosis was based on the clinical findings made by one of three neurologists attached to our centre. Radiological findings and the presence of either IgM or IgG anticardiolipin antibodies, IgG anti-beta-2 glycoprotein 1 antibodies or a lupus anticoagulant were then documented. In this group of patients three subgroups were identified:1. Individuals that fulfilled the Sapporo Classification Criteria2. Individuals with transiently positive antiphospholipid antibodies and3. Individuals with persistently low positive antiphospholipid antibodies. The most interesting of these three groups are those individuals with transiently positive antiphospholipid antibodies. A potential cause for presentation was identified in only one patient of this group with documented infective endocarditis and bacteraemia. Comparison with the other two groups suggested that there was little in terms of clinical presentation, radiological findings or intercurrent risk factors for thrombotic disease to distinguish between them. With disappearance of antiphospholipid antibodies, the individuals within this group have not had further thrombotic events. Our observations emphasise the problems that continue to exist in relation to the occurrence of cerebrovascular disease in the context of antiphospholipid antibodies and the optimal management of these stratified groups. Our findings also raise an as yet unanswered question as to the signficance of these transiently positive antiphospholipid antibodies. In the absence of significant intercurrent risk factors our findings would suggest that in the group we describe that they are likely to be of clinical significance.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"3 ","pages":"3"},"PeriodicalIF":0.0,"publicationDate":"2006-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-3-3","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25937754","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":"Endothelial cell activation and neovascularization are prominent in dermatomyositis.","authors":"Kanneboyina Nagaraju,&nbsp;Lisa G Rider,&nbsp;Chenguang Fan,&nbsp;Yi-Wen Chen,&nbsp;Megan Mitsak,&nbsp;Rashmi Rawat,&nbsp;Kathleen Patterson,&nbsp;Cecilia Grundtman,&nbsp;Frederick W Miller,&nbsp;Paul H Plotz,&nbsp;Eric Hoffman,&nbsp;Ingrid E Lundberg","doi":"10.1186/1740-2557-3-2","DOIUrl":"https://doi.org/10.1186/1740-2557-3-2","url":null,"abstract":"<p><strong>Background: </strong>While vascular and immune abnormalities are common in juvenile and adult dermatomyositis (DM), the molecular changes that contribute to these abnormalities are not clear. Therefore, we investigated pathways that facilitate new blood vessel formation and dendritic cell migration in dermatomyositis.</p><p><strong>Methods: </strong>Muscle biopsies from subjects with DM (9 children and 6 adults) and non-myositis controls (6 children and 7 adults) were investigated by immunohistochemistry using antibodies that recognize existing (anti-CD146) and newly formed blood vessels (anti-alphaVbeta3) and mature dendritic cells (anti-DC-LAMP). Blood vessel quantification was performed by digitalized image analysis. Additional muscle biopsies from subjects with adult DM and non-myositis controls were used for global gene expression profiling experiments.</p><p><strong>Results: </strong>A significant increase in neovascularization was found in muscle biopsies of DM patients; neovascularization (alphaVbeta3 positive capillaries and vessels per muscle fiber) was much higher in juvenile than in adult DM patients (control vs juvenile DM: Mean +/- SE: 0.06 +/- 0.01 vs 0.6 +/- 0.05; p < 0.0001 and control vs adult DM: Mean +/- SE: 0.60 +/- 0.1 vs 0.75 +/- 0.1; p = 0.051). Gene expression analysis demonstrated that genes that participate not only in angiogenesis but also in leukocyte trafficking and the complement cascade were highly up regulated in DM muscle in comparison to age matched controls. DC-LAMP positive dendritic cells were highly enriched at perivascular inflammatory sites in juvenile and adult DM patients along with molecules that facilitate dendritic cell transmigration and reverse transmigration (CD142 and CD31).</p><p><strong>Conclusion: </strong>These results suggest active neovascularization and endothelial cell activation in both juvenile and adult DM. It is likely that close association of monocytes with endothelial cells initiate rapid dendritic cell maturation and an autoimmune response in DM.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"3 ","pages":"2"},"PeriodicalIF":0.0,"publicationDate":"2006-02-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-3-2","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25877778","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":"Virus-mediated autoimmunity in Multiple Sclerosis.","authors":"Nikolaos Grigoriadis,&nbsp;Georgios M Hadjigeorgiou","doi":"10.1186/1740-2557-3-1","DOIUrl":"https://doi.org/10.1186/1740-2557-3-1","url":null,"abstract":"<p><p>Epidemiological data suggest the notion that in Multiple Sclerosis (MS) is an acquired autoimmune disease and the cause may be an environmental factor(s), probably infectious, in genetically susceptible individuals. Several cases of viral induced demyelinatimg encephalomyelitis in human beings and in experimental models as well as the presence of IgG oligoclonal bands in the cerebrospinal fluid indicate that the infectious factor may be viral. However, the absence of a specific virus identification in MS central nervous system may hardly support this notion. On the other hand, the partial response of patients with MS to immunosuppressive and immunomodulatory therapy support the evidence of an autoimmune etiology for MS. However, the autoimmune hypothesis shares the same criticism with the infectious one in that no autoantigen(s) specific to and causative for MS has ever been identified. Nevertheless, the absence of identifiable infectious agent, especially viral does not rule out its presence at a certain time--point and the concomitant long term triggering of an autoimmune cascade of events thereafter. Several concepts have emerged in an attempt to explain the autoimmune mechanisms and ongoing neurodegeneration in MS on the basis of the infectious--viral hypothesis.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"3 ","pages":"1"},"PeriodicalIF":0.0,"publicationDate":"2006-02-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-3-1","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25877844","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":"Phenytoin as a novel anti-vitiligo weapon.","authors":"M R Namazi","doi":"10.1186/1740-2557-2-11","DOIUrl":"https://doi.org/10.1186/1740-2557-2-11","url":null,"abstract":"<p><p>Vitiligo is a psychologically devastating clinical conundrum which affects approximately 1% of the general population. The exact cause of the illness is an enigma, but several hypotheses about its pathogenesis are advanced. The autoimmune hypothesis proposes an autoimmune attack against melanocytes. Although anti-melanocyte autoantibodies have been demonstrated in vitiligo, recent research casts doubt on their pathogenic role and instead supports the involvement of cell-mediated autoimmune response in the pathobiology of this disorder, which is characterized by increase of suppressor T-cells and decrease of the helper/suppressor ratio in association with the presence of type-1 cytokine secreting cytotoxic T cells in the vicinity of disappearing melanocytes. The neural hypothesis proposes that increased release of norepinephrine, a melanocytotoxin, from the autonomic nerve endings in the microenvironment of melanocytes injures these cells. Moreover, norepinephrine induces the catecholamine degrading enzyme monoamine oxidase (MAO), which favors the formation of toxic levels of hydrogen peroxide in the vicinity of melanocytes. Another theory suggests that abnormal permeability of melanosome membrane, which normally prevents the diffusion of toxic melanin precursors into the cytoplasm, may cause melanocyte damage. Phenytoin, the widely-used anticonvulsant, has been employed both topically and systemically in the treatment of some dermatological disorders. The drug has been shown to significantly suppress mitogen-induced activation of lymphocytes and cytotoxic T lymphocyte activity and to polarize the immune response toward the type-2 pathway. It also significantly decreases suppressor T cells and increases the helper/suppressor ratio. At high concentrations, the drug inhibits the release of norepinephrine and the activity of MAO. Moreover, phenytoin is suggested to interact with membrane lipids, which may promote stabilization of the membranes. The hydantoin moiety of phenytoin exerts a direct stimulatory action on melanocytes; facial hyperpigmentation is a recognized side effect of orally administered phenytoin. Altogether, the above evidence suggests that phenytoin could be therapeutically effective against vitiligo. As phenytoin stimulates collagen production and inhibits its breakdown, its concomitant use with topical steroids could prevent steroid-induced skin atrophy while potentiating the anti-vitiligo effect of these agents.</p>","PeriodicalId":87189,"journal":{"name":"Journal of autoimmune diseases","volume":"2 ","pages":"11"},"PeriodicalIF":0.0,"publicationDate":"2005-11-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1186/1740-2557-2-11","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"25700188","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}