The Open autoimmunity journal最新文献

筛选
英文 中文
Editorial- Dual and Opposite Actions of Cytokines in Autoimmune Inflammatory Demyelination 编辑-细胞因子在自身免疫性炎症性脱髓鞘中的双重和相反作用
The Open autoimmunity journal Pub Date : 2010-07-14 DOI: 10.2174/1876894601002040139
B. Gran, B. Becher
{"title":"Editorial- Dual and Opposite Actions of Cytokines in Autoimmune Inflammatory Demyelination","authors":"B. Gran, B. Becher","doi":"10.2174/1876894601002040139","DOIUrl":"https://doi.org/10.2174/1876894601002040139","url":null,"abstract":"The biological actions of cytokines in the immune system and specifically in autommunity have been carefully studied in the last few decades [1], in particular after Mosmann and Coffman observed that certain T helper cell populations could be categorised based on the cytokines they produce [2]. It was perhaps inevitable that progress in our knowledge of cytokine biology would generate simplified paradigms that have been challenged and refined over time. In the early stages of the definition of Th1 and Th2 cells, it was readily acknowledged by Mosmann and Coffman that “Further divisions of helper T cells may have to be recognized before a complete picture of helper T-cell function can be obtained” [3] and this is indeed what happened when Th3 [4] and more recently Th17 [5-7], Th9 [8, 9], and Th22 [10] subsets were recognised. While Th1, Th2 and regulatory T cells display a high degree of stability and can even enter the pool of memory cells, Th17 and other newly described populations appear to not truly represent a stable committed lineage. It now appears most likely that significant plasticity in T cell function enables them to produce even more varied combinations of cytokines that are “customised” to the systemic and local requirement of the immune system [11, 12].","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"139-140"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151650","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}
引用次数: 1
IL-22 vs. IL-22: The Tissue Matters~!2009-08-25~!2009-11-04~!2010-07-14~! IL-22与IL-22:组织关系
The Open autoimmunity journal Pub Date : 2010-07-14 DOI: 10.2174/1876894601002040181
Katharina Kreymborg
{"title":"IL-22 vs. IL-22: The Tissue Matters~!2009-08-25~!2009-11-04~!2010-07-14~!","authors":"Katharina Kreymborg","doi":"10.2174/1876894601002040181","DOIUrl":"https://doi.org/10.2174/1876894601002040181","url":null,"abstract":"IL-22 is a cytokine recently discovered to be produced by TH17 cells. Its receptor is expressed in the skin, liver, the digestive and the respiratory tract where IL-22 conveys signals of the immune system directly to the tissue. IL-22 is involved in the host defense against extracellular pathogens as well as in autoimmune inflammatory diseases and exerts, depending on the tissue and inflammatory context, proinflammatory, protective or no evident function. Focusing on im- mune-mediated pathology, here we will discuss the role of IL-22 in the context of tissue inflammation to provide an over- view of the complex properties of this bi-functional cytokine and to disentangle some of its apparently aberrant actions.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"181-186"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151755","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}
引用次数: 10
Diverse and Opposing Roles of IL-27 in Immunity~!2009-11-04~!2009-12-16~!2010-07-14~! IL-27在免疫中的不同和对立作用2009-11-04 2009-12-16 2010-07-14
The Open autoimmunity journal Pub Date : 2010-07-14 DOI: 10.2174/1876894601002040187
Zoe Fonseca-Kelly
{"title":"Diverse and Opposing Roles of IL-27 in Immunity~!2009-11-04~!2009-12-16~!2010-07-14~!","authors":"Zoe Fonseca-Kelly","doi":"10.2174/1876894601002040187","DOIUrl":"https://doi.org/10.2174/1876894601002040187","url":null,"abstract":"IL-27 was originally thought to play a pro-inflammatory role in immunity, however it is now clear that IL-27 also exerts potent anti-inflammatory effects. Here, we discuss some of the key studies that have elucidated the diverse and apparently paradoxical roles of IL-27. While IL-27 can promote early Th1 development there is evidence of suppressive effects in later phases of Th1 responses. IL-27 exerts a direct inhibitory effect in Th2 immunity by blocking Th2 cell dif- ferentiation. The role of IL-27 in Th17 immune responses is also complex as it seems that while IL-27 can block early Th17 development, fully differentiated Th17 cells may become resistant to the inhibitory effects of IL-27. In the field of cancer biology, IL-27 has been shown to have anti-tumourigenic effects however it acts via both immunogenic and non- immunogenic mechanisms. Collectively, the studies discussed in this review have demonstrated multiple biological func- tions and mechanisms of action of IL-27.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"187-192"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151850","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}
引用次数: 4
IL-17A in Autoimmune Inflammation of the Central Nervous System: A Promising Therapeutic Target in Multiple Sclerosis?~!2009-09-21~!2009-10-28~!2010-07-14~! 中枢神经系统自身免疫性炎症中的IL-17A:多发性硬化症的一个有希望的治疗靶点
The Open autoimmunity journal Pub Date : 2010-07-14 DOI: 10.2174/1876894601002040171
B. Ciric
{"title":"IL-17A in Autoimmune Inflammation of the Central Nervous System: A Promising Therapeutic Target in Multiple Sclerosis?~!2009-09-21~!2009-10-28~!2010-07-14~!","authors":"B. Ciric","doi":"10.2174/1876894601002040171","DOIUrl":"https://doi.org/10.2174/1876894601002040171","url":null,"abstract":"Discovery of the IL-23/Th17 axis brought to an end the era of the Th1/Th2 paradigm and radically advanced our understanding of autoimmunity. Experimental autoimmune encephalitis (EAE), an animal model of multiple sclerosis (MS), was highly instrumental in discovery of the IL-23/Th17 axis and the ensuing rapid progress in the field. Despite an early start and subsequent intense focus on the role of this axis in EAE and MS, some basic questions remained controver- sial, such as the role of IL-17A, a signature cytokine of Th17 lineage. Copious production of IL-17A combined with its pro-inflammatory effects offered a plausible explanation for the pronounced encephalitogenicity of Th17 cells. A body of experimental data from a number of laboratories demonstrated its important, if not essential, role in EAE, thus pointing to this cytokine as a promising therapeutic target in MS. Findings that MS lesions contain high percentages of Th17 and Tc17 cells and large quantities of IL-17A, similar to EAE, further supported this view. Unexpectedly, two recent findings raised doubts that IL-17A should still be considered an attractive target in MS: contradictory to previous findings, both overexpression and genetic deficiency or neutralization of IL-17A had no significant effect in EAE; in a clinical trial, treatment with anti-IL-12/23p40 antibody did not have a beneficial effect in MS, which came as a surprise since analo- gous approaches efficaciously suppressed EAE. Here we review findings about the role of IL-17A in EAE, with an em- phasis on its potential as a therapeutic target in MS.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"171-180"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151746","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}
引用次数: 3
A Paradoxical Effect of Systemic IL-23 in EAE – Limitation of Autoimmune Inflammatory Demyelination 系统性IL-23在EAE中的矛盾作用——自身免疫性炎症脱髓鞘的局限性
The Open autoimmunity journal Pub Date : 2010-07-14 DOI: 10.2174/1876894601002040141
T. Touil, N. Chu, U. Bohlmann, P. Bargsten, L. Yonghai, D. Fitzgerald, Guang-Xian Zhang, B. Becher, A. Rostami, B. Gran
{"title":"A Paradoxical Effect of Systemic IL-23 in EAE – Limitation of Autoimmune Inflammatory Demyelination","authors":"T. Touil, N. Chu, U. Bohlmann, P. Bargsten, L. Yonghai, D. Fitzgerald, Guang-Xian Zhang, B. Becher, A. Rostami, B. Gran","doi":"10.2174/1876894601002040141","DOIUrl":"https://doi.org/10.2174/1876894601002040141","url":null,"abstract":"The heterodimeric cytokine IL-23 plays a non-redundant function in the development of cell-mediated, organ- specific autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE). To further characterize the mechanisms of action of IL-23 in autoimmune inflammation, we administered IL-23 systemically at different time points during both relapsing and chronic EAE. Surprisingly, we found suppression of disease in all treatment protocols. We ob- served a reduction in the number of activated macrophages and microglia in the CNS, while T cell infiltration was not significantly affected. Disease suppression correlated with reduced expansion of myelin-reactive T cells, loss of T-bet ex- pression, loss of lymphoid structures, and increased production of IL-6 and IL-4. Here we describe an unexpected func- tion of exogenous IL-23 in limiting the scope and extent of organ-specific autoimmunity.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"11 1","pages":"141-150"},"PeriodicalIF":0.0,"publicationDate":"2010-07-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151696","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}
引用次数: 1
Antiphospholipid Antibodies and Autoimmune Diseases~!2009-10-09~!2009-10-22~!2010-03-11~! 抗磷脂抗体与自身免疫性疾病~!
The Open autoimmunity journal Pub Date : 2010-03-17 DOI: 10.2174/1876894601002020038
G. Remondino, A. Allievi
{"title":"Antiphospholipid Antibodies and Autoimmune Diseases~!2009-10-09~!2009-10-22~!2010-03-11~!","authors":"G. Remondino, A. Allievi","doi":"10.2174/1876894601002020038","DOIUrl":"https://doi.org/10.2174/1876894601002020038","url":null,"abstract":"","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"38-44"},"PeriodicalIF":0.0,"publicationDate":"2010-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151920","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}
引用次数: 1
Clinical Management of Antiphospholipid Syndrome-Related Thrombosis~!2009-09-14~!2009-09-17~!2010-03-11~! 抗磷脂综合征相关血栓形成的临床处理2009-09-14 2009-09-17 2010-03-11
The Open autoimmunity journal Pub Date : 2010-03-17 DOI: 10.2174/1876894601002020067
G. Espinosa, R. Cervera
{"title":"Clinical Management of Antiphospholipid Syndrome-Related Thrombosis~!2009-09-14~!2009-09-17~!2010-03-11~!","authors":"G. Espinosa, R. Cervera","doi":"10.2174/1876894601002020067","DOIUrl":"https://doi.org/10.2174/1876894601002020067","url":null,"abstract":"","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"67-75"},"PeriodicalIF":0.0,"publicationDate":"2010-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151556","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}
引用次数: 1
Critical Update of the Antiphospholipid Syndrome Criteria~!2009-10-17~!2009-10-20~!2010-03-11~! 抗磷脂综合征标准的重要更新2009-10-17 2009-10-20 2010-03-11
The Open autoimmunity journal Pub Date : 2010-03-17 DOI: 10.2174/1876894601002020018
V. Pengo, A. Ruffatti
{"title":"Critical Update of the Antiphospholipid Syndrome Criteria~!2009-10-17~!2009-10-20~!2010-03-11~!","authors":"V. Pengo, A. Ruffatti","doi":"10.2174/1876894601002020018","DOIUrl":"https://doi.org/10.2174/1876894601002020018","url":null,"abstract":"","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"18-20"},"PeriodicalIF":0.0,"publicationDate":"2010-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151418","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}
引用次数: 4
Antigen Specificity of Antiphospholipid Syndrome-Related Antiphospholipid Antibodies~!2009-09-28~!2009-11-02~!2010-03-11~! 抗磷脂综合征相关抗磷脂抗体抗原特异性研究
The Open autoimmunity journal Pub Date : 2010-03-11 DOI: 10.2174/1876894601002020021
R. Forastiero
{"title":"Antigen Specificity of Antiphospholipid Syndrome-Related Antiphospholipid Antibodies~!2009-09-28~!2009-11-02~!2010-03-11~!","authors":"R. Forastiero","doi":"10.2174/1876894601002020021","DOIUrl":"https://doi.org/10.2174/1876894601002020021","url":null,"abstract":"The antiphospholipid syndrome (APS) is an autoimmune disorder characterized by the presence of antiphos- pholipid antibodies (aPL) and clinically by vascular thrombosis and/or recurrent pregnancy morbidity. The APS- associated aPL are mostly directed against � 2-glycoprotein I (� 2GPI) and prothrombin. In contrast, aPL linked to infec- tious disorders are primarily directed against phospholipids and do not tend to be associated with the clinical manifesta- tions of APS. This distinction, however, was later found not to be absolute. Patients with lepromatous leprosy have a high prevalence of true antibodies to � 2GPI, but they do not develop thromboembolic complications. Current evidence suggests that autoantibodies to � 2GPI from APS patients preferentially bind to critical epitopes in domain I of � 2GP1, and leprosy- related aPL recognizing � 2GPI tend to be directed against domain V. The position of the epitope in the � 2GPI molecule seems to be crucial in defining the pathogenicity of aPL. In addition, an increasing number of other phospholipids-binding proteins with central functions in the regulation of blood coagulation and fibrinolysis are also targeted by APS-related autoantibodies. This review intends to highlight the diverse antigen specificity of aPL and likely further studies would help to understand the different clinical behavior of patients with APS and infections-related aPL.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"21-27"},"PeriodicalIF":0.0,"publicationDate":"2010-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151437","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}
引用次数: 3
A Comprehensive Review of Thrombogenic Mechanisms in APS~!2009-10-13~!2009-10-19~!2010-03-11~! APS血栓形成机制综述2009-10-13 2009-10-19 2010-03-11
The Open autoimmunity journal Pub Date : 2010-03-11 DOI: 10.2174/1876894601002020058
Renan A Aguilar-valenzuela, L. Martínez-Martínez, S. Pierangeli
{"title":"A Comprehensive Review of Thrombogenic Mechanisms in APS~!2009-10-13~!2009-10-19~!2010-03-11~!","authors":"Renan A Aguilar-valenzuela, L. Martínez-Martínez, S. Pierangeli","doi":"10.2174/1876894601002020058","DOIUrl":"https://doi.org/10.2174/1876894601002020058","url":null,"abstract":"The antiphospholipid syndrome (APS) is an acquired thombophilia, which is characterized by one or more thrombotic episodes and obstetric complications in the presence of antiphospholipid (aPL) antibodies (Abs). aPL Abs are detected by laboratory tests such as lupus anticoagulant (LA), anticardiolipin (aCL) and anti- 2-glycoprotein I ( 2GPI) Abs. This article reviews the most current pathophysiological aspects of APS with emphasis in thrombotic and pro- inflammatory mechanisms mediated by aPL antibodies.","PeriodicalId":89633,"journal":{"name":"The Open autoimmunity journal","volume":"2 1","pages":"58-66"},"PeriodicalIF":0.0,"publicationDate":"2010-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"68151546","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}
引用次数: 4
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信