Pub Date : 2022-01-01DOI: 10.1016/b978-0-12-822564-6.00016-1
H. Ahsan, M Zahid Hasan, R. Ahmad
{"title":"Role of free radicals in autoimmune diseases","authors":"H. Ahsan, M Zahid Hasan, R. Ahmad","doi":"10.1016/b978-0-12-822564-6.00016-1","DOIUrl":"https://doi.org/10.1016/b978-0-12-822564-6.00016-1","url":null,"abstract":"","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76907039","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}
Pub Date : 2022-01-01DOI: 10.1016/b978-0-12-822564-6.00019-7
M. Cook
{"title":"Regulation of immunological tolerance and human autoimmunity by NF-κB","authors":"M. Cook","doi":"10.1016/b978-0-12-822564-6.00019-7","DOIUrl":"https://doi.org/10.1016/b978-0-12-822564-6.00019-7","url":null,"abstract":"","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85375204","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}
Pub Date : 2022-01-01DOI: 10.1016/b978-0-12-822564-6.00015-x
S. Elfishawi, M. Elfishawi
{"title":"Human leukocyte antigen and autoimmunity","authors":"S. Elfishawi, M. Elfishawi","doi":"10.1016/b978-0-12-822564-6.00015-x","DOIUrl":"https://doi.org/10.1016/b978-0-12-822564-6.00015-x","url":null,"abstract":"","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83116131","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}
Pub Date : 2022-01-01DOI: 10.1016/b978-0-12-822564-6.00020-3
G. Ramponi, E. Brunetta, M. Folci
{"title":"Role of Th1 and Th2 in autoimmunity","authors":"G. Ramponi, E. Brunetta, M. Folci","doi":"10.1016/b978-0-12-822564-6.00020-3","DOIUrl":"https://doi.org/10.1016/b978-0-12-822564-6.00020-3","url":null,"abstract":"","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88894117","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}
Pub Date : 2022-01-01DOI: 10.1016/b978-0-12-822564-6.09992-4
{"title":"Copyright","authors":"","doi":"10.1016/b978-0-12-822564-6.09992-4","DOIUrl":"https://doi.org/10.1016/b978-0-12-822564-6.09992-4","url":null,"abstract":"","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87132881","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}
Pub Date : 2022-01-01DOI: 10.1016/b978-0-12-824390-9.09993-x
{"title":"Index","authors":"","doi":"10.1016/b978-0-12-824390-9.09993-x","DOIUrl":"https://doi.org/10.1016/b978-0-12-824390-9.09993-x","url":null,"abstract":"","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85678327","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}
Pub Date : 2022-01-01DOI: 10.1016/j.jtauto.2022.100170
Iván Posso-Osorio , Lady J. Rios-Serna , Angie M. Rosero , Diana Cárdenas , Gabriel J. Tobón , Carlos A. Cañas
We report a case of 65-year-old male patient with primary hyperparathyroidism (PHPT) who was admitted to the hospital for autoimmune manifestations (including autoimmune hepatitis and autoantibody development) and exhibited subsequent clinical and paraclinical improvement after parathyroidectomy. By flow cytometry, the expression of PTH receptor 1 (PTHR1) on B lymphocytes of peripheral blood was documented to be higher than that in healthy controls. After parathyroidectomy, autoimmune manifestations improved, while PTH1R expression on B-lymphocytes increased. The possible role of the dynamics of B-lymphocyte PTHR1 in the development of this autoimmune phenomenon is discussed.
{"title":"Improvement of the autoimmune phenomenon after treatment of primary hyperparathyroidism: Possible role of dynamics of parathyroid hormone-1-receptor in B-lymphocytes","authors":"Iván Posso-Osorio , Lady J. Rios-Serna , Angie M. Rosero , Diana Cárdenas , Gabriel J. Tobón , Carlos A. Cañas","doi":"10.1016/j.jtauto.2022.100170","DOIUrl":"10.1016/j.jtauto.2022.100170","url":null,"abstract":"<div><p>We report a case of 65-year-old male patient with primary hyperparathyroidism (PHPT) who was admitted to the hospital for autoimmune manifestations (including autoimmune hepatitis and autoantibody development) and exhibited subsequent clinical and paraclinical improvement after parathyroidectomy. By flow cytometry, the expression of PTH receptor 1 (PTHR1) on B lymphocytes of peripheral blood was documented to be higher than that in healthy controls. After parathyroidectomy, autoimmune manifestations improved, while PTH1R expression on B-lymphocytes increased. The possible role of the dynamics of B-lymphocyte PTHR1 in the development of this autoimmune phenomenon is discussed.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/4f/f4/main.PMC9638815.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40674565","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}
Pub Date : 2022-01-01DOI: 10.1016/j.jtauto.2022.100171
Lorenz Thurner , Natalie Fadle , Evi Regitz , Klaus-Dieter Preuss , Frank Neumann , Onur Cetin , Claudia Schormann , Marie-Christin Hoffmann , Christian Herr , Parastoo Kheiroddin , Torben Millard Rixecker , Robert Bals , Sylviane Muller , Bernhard Thurner , Christoph Kessel , Michael Kabesch , Moritz Bewarder , Kristina Heyne , Christian Lensch , Igor Age Kos
Long COVID is a collection of symptoms as a late sequelae of SARS-CoV-2 infection. It often includes mental symptoms such as cognitive symptoms, persisting loss of smell and taste, in addition to exertional dyspnea. A role of various autoantibodies (autoAbs) has been postulated in long-COVID and is being further investigated. With the goal of identifying potentially unknown autoAbs, we screened plasma of patients with long COVID on in-house post-translationally modified protein macroarrays including citrullinated, SUMOylated and acetylated membranes. SUMO1ylated isoform DEAD/H (Asp-Glu-Ala-Asp/His) box helicase 35 (SUMO1-DHX35) was identified as only candidate antigen. In adult patients with long COVID, IgG autoAbs against SUMO1-DHX35 of IgG class were found in seven of 71 (9.8%) plasma samples, of IgM and IgG class in one of 69 (1.4%) samples, not in 200 healthy adult controls, not in 442 healthy children, and 146 children after SARS-CoV-2 infection. All autoAb-positive seven patients were female. AutoAb titers ranged between 200 to up to 400 By point mutagenesis and expression of FLAG-tagged mutants of DHX35 in HEK293 cells, and subsequent SUMOylation of purified constructs, lysine 53 was identified as a unique, never yet identified, SUMOylation site. The autoAbs had no reactivity against the non-SUMO1ylated mutant (K53R) of DHX35. To summarize, autoAbs against SUMO1-DHX35 were identified in adult female patients with long-COVID. Further studies are needed to verify the frequency of occurrence. The function of DHX35 has not yet been determined and there is no available information in relation to disease implication. The molecular mechanism causing the SUMOylation, the potential functional consequences of this post-translational modification on DHX35, and a potential pathogenicity of the autoAbs against SUMO1-DHX35 in COVID-19 and other possible contexts remain to be elucidated.
长冠状病毒是SARS-CoV-2感染晚期后遗症的症状集合。它通常包括精神症状,如认知症状,持续的嗅觉和味觉丧失,以及用力性呼吸困难。多种自身抗体(autoAbs)在长期covid中的作用已被假设,并正在进一步研究。为了鉴定潜在未知的自身抗体,我们使用内部翻译后修饰的蛋白大阵列(包括瓜氨酸化、SUMOylated和乙酰化膜)筛选长COVID患者的血浆。唯一的候选抗原为sumo1 - glu - ala - asp /His盒解旋酶35 (SUMO1-DHX35)。在成年长COVID患者中,71份血浆样本中有7份(9.8%)检测到IgG类抗体,69份(1.4%)血浆样本中有1份(1.4%)检测到IgM和IgG类抗体,200名健康成人对照、442名健康儿童和146名SARS-CoV-2感染后的儿童中没有检测到抗SUMO1-DHX35抗体。7例自体抗体阳性患者均为女性。通过点诱变和在HEK293细胞中表达DHX35的flag标记突变体,并随后对纯化的构建体进行SUMOylation,鉴定出赖氨酸53是一个独特的,从未被鉴定过的SUMOylation位点。自身抗体对DHX35非sumo1化突变体(K53R)无反应性。综上所述,在成年女性长covid患者中检测到针对SUMO1-DHX35的自身抗体。需要进一步的研究来验证发生的频率。DHX35的功能尚未确定,也没有与疾病相关的可用信息。导致SUMO1-DHX35磷酸化的分子机制、这种翻译后修饰对DHX35的潜在功能影响,以及自身抗体在COVID-19和其他可能的情况下对SUMO1-DHX35的潜在致病性仍有待阐明。
{"title":"Autoantibodies against SUMO1-DHX35 in long-COVID","authors":"Lorenz Thurner , Natalie Fadle , Evi Regitz , Klaus-Dieter Preuss , Frank Neumann , Onur Cetin , Claudia Schormann , Marie-Christin Hoffmann , Christian Herr , Parastoo Kheiroddin , Torben Millard Rixecker , Robert Bals , Sylviane Muller , Bernhard Thurner , Christoph Kessel , Michael Kabesch , Moritz Bewarder , Kristina Heyne , Christian Lensch , Igor Age Kos","doi":"10.1016/j.jtauto.2022.100171","DOIUrl":"10.1016/j.jtauto.2022.100171","url":null,"abstract":"<div><p>Long COVID is a collection of symptoms as a late sequelae of SARS-CoV-2 infection. It often includes mental symptoms such as cognitive symptoms, persisting loss of smell and taste, in addition to exertional dyspnea. A role of various autoantibodies (autoAbs) has been postulated in long-COVID and is being further investigated. With the goal of identifying potentially unknown autoAbs, we screened plasma of patients with long COVID on in-house post-translationally modified protein macroarrays including citrullinated, SUMOylated and acetylated membranes. SUMO1ylated isoform DEAD/H (Asp-Glu-Ala-Asp/His) box helicase 35 (SUMO1-DHX35) was identified as only candidate antigen. In adult patients with long COVID, IgG autoAbs against SUMO1-DHX35 of IgG class were found in seven of 71 (9.8%) plasma samples, of IgM and IgG class in one of 69 (1.4%) samples, not in 200 healthy adult controls, not in 442 healthy children, and 146 children after SARS-CoV-2 infection. All autoAb-positive seven patients were female. AutoAb titers ranged between 200 to up to 400 By point mutagenesis and expression of FLAG-tagged mutants of DHX35 in HEK293 cells, and subsequent SUMOylation of purified constructs, lysine 53 was identified as a unique, never yet identified, SUMOylation site. The autoAbs had no reactivity against the non-SUMO1ylated mutant (K53R) of DHX35. To summarize, autoAbs against SUMO1-DHX35 were identified in adult female patients with long-COVID. Further studies are needed to verify the frequency of occurrence. The function of DHX35 has not yet been determined and there is no available information in relation to disease implication. The molecular mechanism causing the SUMOylation, the potential functional consequences of this post-translational modification on DHX35, and a potential pathogenicity of the autoAbs against SUMO1-DHX35 in COVID-19 and other possible contexts remain to be elucidated.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/bb/06/main.PMC9675633.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40494182","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}
Pub Date : 2022-01-01DOI: 10.1016/j.jtauto.2022.100165
Niels Hansen
N-Methyl-d-Aspartate-receptor (NMDAR) antibody encephalitis is a disease discovered two decades ago. Our knowledge about it has recently deepened dramatically. However, the significance of NMDAR antibodies in psychiatric disease cannot be determined if there are no clear indications of brain inflammation or an autoimmune encephalitis mediated by NMDAR antibodies. Furthermore, the long-term interaction and connection between these two disease entities are unclear. In this paper we aim to elucidate the relationship between these disease entities. We propose two distinct models that explain the on the one hand a condition in which a minor inflammatory state as in psychiatric disease culminates in a severe state of inflammation characterized by NMDAR encephalitis. On the other hand, we postulate a model in which an NMDAR encephalitis might later create favorable conditions for inducing psychiatric disease. These models should be kept in mind for further investigations examining the long-term outcome of NMDAR autoantibody immunity in the brain and its functions.
n -甲基-d-天冬氨酸受体(NMDAR)抗体脑炎是20年前发现的一种疾病。我们对它的了解最近急剧加深。然而,如果没有明确的脑炎或由NMDAR抗体介导的自身免疫性脑炎的适应症,则无法确定NMDAR抗体在精神疾病中的意义。此外,这两种疾病之间的长期相互作用和联系尚不清楚。在本文中,我们旨在阐明这些疾病实体之间的关系。我们提出了两种不同的模型,一方面解释了精神疾病中轻微的炎症状态最终以NMDAR脑炎为特征的严重炎症状态。另一方面,我们假设NMDAR脑炎可能后来为诱发精神疾病创造有利条件的模型。为了进一步研究NMDAR自身抗体免疫在大脑中的长期结果及其功能,应该记住这些模型。
{"title":"NMDAR autoantibodies in psychiatric disease - An immunopsychiatric continuum and potential predisposition for disease pathogenesis","authors":"Niels Hansen","doi":"10.1016/j.jtauto.2022.100165","DOIUrl":"10.1016/j.jtauto.2022.100165","url":null,"abstract":"<div><p><em>N</em>-Methyl-<span>d</span>-Aspartate-receptor (NMDAR) antibody encephalitis is a disease discovered two decades ago. Our knowledge about it has recently deepened dramatically. However, the significance of NMDAR antibodies in psychiatric disease cannot be determined if there are no clear indications of brain inflammation or an autoimmune encephalitis mediated by NMDAR antibodies. Furthermore, the long-term interaction and connection between these two disease entities are unclear. In this paper we aim to elucidate the relationship between these disease entities. We propose two distinct models that explain the on the one hand a condition in which a minor inflammatory state as in psychiatric disease culminates in a severe state of inflammation characterized by NMDAR encephalitis. On the other hand, we postulate a model in which an NMDAR encephalitis might later create favorable conditions for inducing psychiatric disease. These models should be kept in mind for further investigations examining the long-term outcome of NMDAR autoantibody immunity in the brain and its functions.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9513762/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"40383464","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}
Pub Date : 2022-01-01DOI: 10.1016/j.jtauto.2022.100150
Nancy P. Duarte-Delgado , Mónica P. Cala , Alfonso Barreto , Luz-Stella Rodríguez C
Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are chronic autoimmune diseases that result from the combined influence of genetic and environmental factors that promotes the loss of tolerance to cellular components. The complexity of these diseases converts them into a major challenge at the diagnostic and treatment level. Therefore, it is convenient to implement the use of tools for a better understanding of the physiopathology of these diseases to propose reliable biomarkers. The “omics” disciplines like metabolomics and lipidomics allow to study RA and SLE in a higher degree of detail since they evaluate the metabolites and metabolic pathways involved in disease pathogenesis. This review has compiled the information of metabolomics and lipidomics studies where samples obtained from RA and SLE patients were evaluated to find the metabolites and pathways differences between patients and healthy controls. In both diseases, there is a decrease in several amino acids and oxidative stress-related metabolites like glutathione. These findings may be useful for functional metabolomics studies aiming to reprogram the metabolism in a disease setting to recover normal immune cell homeostasis and function.
{"title":"Metabolites and metabolic pathways associated with rheumatoid arthritis and systemic lupus erythematosus","authors":"Nancy P. Duarte-Delgado , Mónica P. Cala , Alfonso Barreto , Luz-Stella Rodríguez C","doi":"10.1016/j.jtauto.2022.100150","DOIUrl":"10.1016/j.jtauto.2022.100150","url":null,"abstract":"<div><p>Rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) are chronic autoimmune diseases that result from the combined influence of genetic and environmental factors that promotes the loss of tolerance to cellular components. The complexity of these diseases converts them into a major challenge at the diagnostic and treatment level. Therefore, it is convenient to implement the use of tools for a better understanding of the physiopathology of these diseases to propose reliable biomarkers. The “omics” disciplines like metabolomics and lipidomics allow to study RA and SLE in a higher degree of detail since they evaluate the metabolites and metabolic pathways involved in disease pathogenesis. This review has compiled the information of metabolomics and lipidomics studies where samples obtained from RA and SLE patients were evaluated to find the metabolites and pathways differences between patients and healthy controls. In both diseases, there is a decrease in several amino acids and oxidative stress-related metabolites like glutathione. These findings may be useful for functional metabolomics studies aiming to reprogram the metabolism in a disease setting to recover normal immune cell homeostasis and function.</p></div>","PeriodicalId":36425,"journal":{"name":"Journal of Translational Autoimmunity","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2022-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2589909022000119/pdfft?md5=2abddc594b51821c7b9a93f98789b40b&pid=1-s2.0-S2589909022000119-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48317051","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}