The Open autoimmunity journal最新文献

{"title":"Relationship between Autoimmunity and Cancer or Metabolic Abnormality in Liver Diseases","authors":"T. Himoto, M. Nishioka, T. Masaki","doi":"10.2174/1876894601406010001","DOIUrl":"https://doi.org/10.2174/1876894601406010001","url":null,"abstract":"Recent advances in the serological analysis of recombinant cDNA expression libraries and proteomic analysis have enabled the identification of numerous kinds of novel autoantigens, especially tumor-associated antigens (TAAs). The emergence of antibodies to TAAs might imply that an autoimmune response was involved in the malignant transfor- mation. These autoantibodies to TAAs often have predictive value as well as diagnostic relevance. Similarly, the relation- ship between autoimmunity and metabolic abnormalities, including insulin resistance and hepatic steatosis, has been also documented. Metabolic abnormalities are frequently associated with autoimmune diseases. In contrast, autoimmune reac- tions were occasionally involved in the process of metabolic dysregulation. This review primarily focuses on the current trends for the relationship between autoimmunity and cancer or metabolic abnormalities in liver disease and the current interpretations of autoantibodies in those diseases.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"6 1","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2014-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68152131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"T Cell Receptor Variable Regions in Diabetes Bind to Each Other, to Insulin, Glucagon or Insulin Receptor, and to Their Antibodies","authors":"R. Root-Bernstein, Abigail Podufaly","doi":"10.2174/1876894601204010010","DOIUrl":"https://doi.org/10.2174/1876894601204010010","url":null,"abstract":"Our objective is to elucidate the nature of the autoimmune disregulation in diabetes through the antigen speci- ficity of the T-cell receptor (TCR) sequences generated by patients with type 1 diabetes mellitus (T1DM). Previously we demonstrated that TCR from T1DM patients and NOD mice mimic insulin, glucagon and their receptors. We hypothesize that these TCR will bind to each other (as insulin and glucagon do to their receptors) and also be targets of anti-insulin and anti-glucagon antibodies. The hypervariable regions of multiple TCR from three patients were synthesized and their binding specificities determined using UV spectroscopy. ELISA was used to determine whether these TCR were recog- nized by anti-insulin and anti-glucagon antibodies. Each patient produced TCR that recognized insulin, glucagon and the insulin receptor (IR). These TCR also recognized each other as complementary (possibly idiotype-antiidiotype) pairs. In addition, each TCR peptide was recognized with nanomolar affinity as an antigen by an antibody against insulin, gluca- gon, and/or IR. Finally, each of the antibodies against insulin, glucagon and IR formed a complementary antibody (or idiotype-antiidiotype) pair with another antibody involved in the disease, again at nanomolar affinities. Every possible ex- pression of complementarity (or idiotype-antiidiotype cross-reactivity) involving TCRs and antibodies was manifested by each patient. Two interpretations of these observations are offered. One, following Marchelonis, is that TCR-antibody complementarity is a mechanism for down-regulating the autoimmune process to re-establish tolerance to self-antigens. A non-exclusive alternative is that the trigger for autoimmunity is antigenic complementarity, which results in the produc- tion of complementary TCR and antibodies that appear to have idiotype-antiidiotype relationships among themselves.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"4 1","pages":"10-22"},"PeriodicalIF":0.0,"publicationDate":"2012-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68152121","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cell mediated Immunity Against Three Eye Muscle Antigens and Correlation with Eye Signs in Patients with Transient and Chronic Thyroiditis","authors":"Bao Nguyen, B. Gopinath, G. Ma, B. Champion, J. Wall","doi":"10.2174/1876894601204010004","DOIUrl":"https://doi.org/10.2174/1876894601204010004","url":null,"abstract":"Background: Mild eye signs, especially itchiness and grittiness of the eyelids and upper eyelid retraction (UER), are found in about 25% of patients with Hashimoto's thyroiditis (HT) in whom antibodies against calsequestrin and flavoprotein (Fp) are often detected. The role of T lymphocyte reactivity against eye muscle antigens in patients with thyroiditis has not been investigated. Methods: We studied peripheral blood T lymphocyte reactivity against calsequestrin, Flavoprotein (Fp) and G2s in pa- tients with transient (sub acute and silent) thyroiditis (TT) and HT, determined in a standard proliferation assay. Reactivity was expressed as stimulation index (SI) and correlated with signs of ophthalmopathy and upper eyelid disease, assessed as; NOSPECS classes, clinical activity score (CAS) and upper eyelid retraction (UER). Results: Positive lymphocyte proliferation to calsequestrin was demonstrated in 71% of TT patients all of whom had mild ophthalmopathy and this was significantly increased compared to normal control subjects. The prevalences of positive T cell reactivity to calsequestrin was also significantly increased in HT patients (38%) compared to the controls, all of whom had upper eyelid disease. Three out of 7 patients with upper eyelid disease (6 of the patients with TT or HT and one other patient with Graves' disease) taken as a separate group, demonstrated significant T lymphocyte sensitisation to cal- sequestrin. TSH-receptor antibodies were detected in only one TT patient and one patient with upper eyelid disease. Interpretation: The development of ophthalmopathy and/or eyelid retraction (in the absence of TSH-r antibodies and Graves' hyperthyroidism) in TT patients is closely associated with an autoimmune reaction against calsequestrin. These findings support the notion that ophthalmopathy and upper eyelid inflammation and dysfunction are independent autoim- mune disorders not necessarily linked with thyroid autoimmunity and that T cell reactivity plays a role.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"4 1","pages":"4-9"},"PeriodicalIF":0.0,"publicationDate":"2012-09-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68152110","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunoblot Assay is Still Useful For the Serological Diagnosis of Autoimmune Bullous Dermatosis","authors":"D. Bertin, C. Leonnet, P. Berbis, D. Gilbert, M. Richard, F. Carsuzaa, J. Grob, S. Desplat-jégo","doi":"10.2174/1876894601204010001","DOIUrl":"https://doi.org/10.2174/1876894601204010001","url":null,"abstract":"The detection of autoantibodies to epidermal or basement membrane zone proteins by immunoblot (IB) is use- ful for the diagnosis and the classification of autoimmune bullous diseases (AIBD). IB using human skin extracts is actu- ally the reference method but A431 cell line is proposed as easier alternate antigen source. We explored the performances of \"A431 IB\" in comparison with the reference technique in retrospectively selected pa- tients suffering from well-established bullous pemphigoid (n=42) or pemphigus vulgaris (n=15) and controls (n=80) in or- der to determine the validity and interest of this simplified IB method. We demonstrated that in our selected population A431 IB performances are comparable to the reference IB. IB remains semi-quantitative and time-consuming but much more economical and informative than commercially available ELISAs. We support the contention that, in 2012, IB, especially A431 IB, is still useful for the serological diagnosis of AIBD.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"4 1","pages":"1-3"},"PeriodicalIF":0.0,"publicationDate":"2012-08-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68152075","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Differential Regulation of CD4+ T Helper Cell Subset Responses by 15-deoxy-Δ12,14-Prostaglandin J2 in Experimental Autoimmune Encephalomyelitis","authors":"Saravanan Kanakasabai, Crystal C. Walline, E. Casalini, C. Mo, W. Chearwae, J. Bright","doi":"10.2174/1876894601103010017","DOIUrl":"https://doi.org/10.2174/1876894601103010017","url":null,"abstract":"Peroxisome proliferator-activated receptor (PPAR) is a family of nuclear receptor transcription factors that regulates immune cell growth, differentiation and homeostasis. We and others have shown earlier that in vivo treatment with PPAR , / or agonists ameliorates experimental autoimmune encephalomyelitis (EAE) model of multiple sclerosis (MS). In this study we show that C57BL/6 mice induced to develop EAE display augmented neural antigen-specific T cell response that was inhibited by PPAR agonist 15-deoxy12,14 -Prostaglandin J2 (15d-PGJ2). EAE mice showed elevated expression of IFN and IL-17 in the CNS and lymphoid organs compared to naïve mice that decreased significantly following treatment with 15d-PGJ2. EAE mice also expressed elevated levels of IL-12 and IL-23 that decreased after treatment with 15d-PGJ2. 15d-PGJ2 also attenuated the expression of IFN , IL-17, IL-12 and IL-23 in neural antigenspecific spleen cells ex vivo and in vitro. Moreover, EAE mice expressed low levels of IL-4, IL-10 and PPAR compared to naïve that increased significantly following treatment with 15d-PGJ2. However, 15d-PGJ2 failed to change the expansion of CD4 + CD25 + Foxp3 + Treg cells in EAE. These findings suggest that 15d-PGJ2 differentially regulates CD4 + T helper cell subset responses in EAE.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"3 1","pages":"17-28"},"PeriodicalIF":0.0,"publicationDate":"2011-12-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68152047","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmune Pancreatitis: An Autoimmune or Immunoinflammatory Disease?","authors":"Yvonne Hsieh, Sudhanshu Agrawal, Leman Yel, Sudhir Gupta","doi":"10.2174/1876894601103010010","DOIUrl":"https://doi.org/10.2174/1876894601103010010","url":null,"abstract":"Autoimmune pancreatitis (AIP) has been widely presumed to be an autoimmune disease that is characterized by elevated IgG and/or IgG4, the presence of autoantibodies, and an infiltration of lymphocytes and plasma cells with fi- brosis. However, no detailed immunological studies have been published. To define immunological changes in AIP in de- tail, and to review evidence for autoimmunity which may be antigen specific and may play a role in the pathogenesis of AIP, and therefore, to determine whether AIP is an autoimmune disease. A detailed immunological investigation for both innate and adaptive immune responses was performed in a patient with AIP. Review of literature was performed from Pub med, and Medline search. Immunological analysis of patient with AIP revealed increased production of proinflammatory IL-6, and IL-17, and increased NK cell activity. No organ-specific or non-specific antibodies were detected. There was no correlation between serum IgG4 with disease activity or response to steroid therapy. Review of literature revealed lack of auto-antigen-specific T and B cell responses in AIP, and autoantibodies are present only in a subset of patients, and are not specific to pancreatic tissue antigens. Therefore, we propose the term Immunoinflammatory pancreatitis rather than an autoimmune pancreatitis. Autoimmune pancreatitis is typically characterized by a diffuse or segmental narrowing of the main pancreatic duct on imaging, elevated IgG and/or IgG4, the presence of autoantibodies, an infiltration of lymphocytes and plasma cells, and presence of fibrosis. The autoantibodies that have been examined include ANA, anti-microsomal antibodies, anti-thyroglobulin antibodies, and antibodies against pancre- atic secretory trypsin inhibitor, lactoferrin, and carbonic an- hydrase (2-5). However, the presence of these autoantibodies has been only sporadically documented in limited numbers of cases. In addition, many of these autoantibodies are di- rected against antigens that are also present in the salivary gland, biliary duct, and distal renal tubules. The detection of IgG, IgG4, antinuclear antibodies, and rheumatoid factor","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"3 1","pages":"10-16"},"PeriodicalIF":0.0,"publicationDate":"2011-12-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Activation of Complement Alternative Pathway in Rheumatoid Arthritis: Implications in Peripheral Neutrophils Functions","authors":"A. B. Paoliello-Paschoalato, M. R. Moreira, A. Azzolini, Amarildo A. Cavenaghi, C. M. Marzocchi-Machado, E. Donadi, A. I. Assis-Pandochi, Y. M. Lucisano-Valim","doi":"10.2174/1876894601103010001","DOIUrl":"https://doi.org/10.2174/1876894601103010001","url":null,"abstract":"Evaluation of the respiratory burst induced by receptors Fc R and CR was carried out in peripheral blood neu- trophils (PBN) in rheumatoid arthritis (RA) patients with active and inactive disease. Simultaneously, cooperation be- tween these receptors and their expression, PBN chemotaxis, and complement system systemic activity were also investi- gated. Neutrophils were stimulated with IC-IgG opsonized with normal human serum (NHS) or not, or with IC-IgG op- sonized with RA human serum (RAHS). ROS production was increased in neutrophils of patients with active or inactive RA stimulated of IC-IgG opsonized with NHS compared to the response of the cells mediated by ICIgG. However, there was poor Fc R/CR cooperation in these RA neutrophils, as indicated by decreased ROS production upon stimulation with IC-IgG opsonized with RAHS. In the case of active RA patients, neutrophils presented significantly higher CR1 and CR3 expression, as well as slight elevation in CD32 and CD16 expression. Positive correlations between Fc R and CR, com- plement alternative pathway activation, and increased RA serum chemotaxic activity were only detected in active RA pa- tients. Taken together, these results indicate that several abnormalities of the complement system exist at the systemic level, namely impaired membrane receptor cooperation, alternative pathway activation, and presence of pre-existing chemoattractant factors in the serum, as reflected by the neutrophil function in the particular case of active RA patients. All, these abnormalities may synergistically contribute to RA pathogenesis.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"17 1","pages":"1-9"},"PeriodicalIF":0.0,"publicationDate":"2011-06-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151865","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TNF-α: A Paradigm of Paradox and Complexity in Multiple Sclerosis and its Animal Models~!2009-10-07~!2009-11-23~!2010-07-14~!","authors":"S. Lim","doi":"10.2174/1876894601002040160","DOIUrl":"https://doi.org/10.2174/1876894601002040160","url":null,"abstract":"TNF-� (tumour necrosis factor-� ) is a pleiotropic cytokine with wide-ranging actions on the immune system and is an important mediator in immune-mediated inflammatory disease states, including multiple sclerosis. TNF-� and its receptors are part of a large and complex superfamily of homologous ligands and receptors, whose many biological func- tions overlap. Investigations have demonstrated the effects of TNF-� at various stages of pathology in multiple sclerosis (MS), including oligodendrocyte death, demyelination, immune cell trafficking, cellular proliferation and major histo- compatibility (MHC) antigen expression. Targeting the TNF-� immunobiological pathway successfully ameliorates dis- ease severity in a number of autoimmune inflammatory conditions except for multiple sclerosis. Anti-TNF-� therapy in experimental autoimmune encephalomyelitis (EAE) showed mixed results, whereas in MS trials it was deleterious. It is clear that TNF-� also has a beneficial role, especially in neuroprotection and regeneration. A clearer understanding of the protective role of TNF-� may be extrapolated from studies in other inflammatory conditions such as stroke and traumatic brain injury.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"160-170"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151740","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Anatomical Colocalization of Vitiligo and Alopecia Areata~!2010-01-18~!2010-05-21~!2010-07-14~!","authors":"M. Rodríguez‐Martín","doi":"10.2174/1876894601002010193","DOIUrl":"https://doi.org/10.2174/1876894601002010193","url":null,"abstract":"","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"193-196"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68152092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Multifaceted Role of Interferon-γ in Central Nervous System Autoimmune Demyelination~!2009-09-01~!2009-11-02~!2010-07-14~!","authors":"L. Sanvito","doi":"10.2174/1876894601002040151","DOIUrl":"https://doi.org/10.2174/1876894601002040151","url":null,"abstract":"Extensive research has been devoted to the study of IFN-� function in several autoimmune diseases. Previously considered the hallmark of Th1 differentiation and pro-inflammatory responses, it has soon become evident that this piv- otal cytokine plays a much more complex role than initially thought. These considerations have been particularly relevant to the understanding of the pathogenesis of autoimmune demyelination of the central nervous system (CNS). Evidence of the multifaceted effects of IFN-� in this disease has been gathered mainly by studies in the animal model, experimental autoimmune encephalomyelitis (EAE). In this review we summarize the fundamental steps and examine the possible fac- tors involved in the apparent dichotomy between pro-inflammatory and protective effects of IFN-� in CNS autoimmune demyelination. A clear understanding of the heterogeneous functions of this key cytokine is paramount in order to fully explore the potential of manipulation of its pathways for the treatment of Multiple Sclerosis.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"151-159"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}