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| 1 | IL-17在局部及全身的致关节炎作用:从发现到靶向治疗显示文摘近年IL-17的重要作用逐渐被全面认识。IL-17主要由辅助性T细胞17(Th17)产生。IL-17家族中有6个成员:IL-A、IL-B、IL-C、IL-D、IL-E(又称IL-25)、IL-F。它可以直接或间接诱导多种细胞因子、炎性因子和抗微生物蛋白介导自身免疫和慢性感染。IL-17在许多自身免疫疾病患者和肿瘤患者中高表达。它涉及多种炎症性疾病的病理过程,包括银屑病、银屑病关节炎、类风湿关节炎、强直性脊柱炎,并在骨丢失和骨形成中起重要作用。目前,多项研究结果为IL-17靶向治疗人类疾病提供了强有力的理论基础。IL-17靶向治疗的相关研究聚焦于控制慢性炎症相关的损伤和疼痛。2015年第一批IL-17靶向抗体被批准用于银屑病的治疗。目前越来越多直接或间接作用于IL-17信号通路的IL-17靶向药物在实验室研究后被用于临床试验。该文综述了IL-17从发现到明确局部和全身致关节炎作用的整个过程,呈现了一个很好的从基础到临床的'转化医学'案例。 | 莫颖倩 毕瑜斐 戴冽 Pierre Miossec | 2018 | 新医学2018，49，7： | 11 |
| 2 | Local and systemic effects of IL-17 in joint inflammation:a historical perspective from discovery to targeting显示文摘The role of IL-17 in many inflammatory and autoimmune diseases is now well established,with three currently registered anti-IL-17-targeted therapies.This story has taken place over a period of 20 years and led to the demonstration that a T cell product could regulate,and often amplify,the inflammatory response.The first results described the contribution of IL-17 to local features in arthritis.Then,understanding was extended to its systemic effects,with a focus on cardiovascular aspects.This review provides a historical perspective of these discoveries focused on arthritis,which started in 1995,followed 10 years later by the description of Th17 cells.Today,IL-17 inhibitors for three chronic inflammatory diseases have been registered.More options are now being tested in ongoing and future clinical trials.Inhibitors of IL-17 family members and Th17 cells ranging from antibodies to small molecules are under active development.The identification of patients with IL-17-driven disease is a key target for the improved selection of patients expected to have a strongly positive response. | Pierre Miossec | 2021 | Cellular & Molecular Immunology2021，18，4： | 5 |
| 3 | Th17 and regulatory T cell balance in autoimmune and inflammatory diseases显示文摘 | Mélissa Noack Pierre Miossec | 2013 | Autoimmunity Reviews2013，，： | 2 |
| 4 | Interleukin-17 and Thl cells: From adult to juve- nile arthritis--Now it is serious显示文摘 | Pierre Miossec | 2011 | Arthritis & Rheumatism2011，63，8： | 1 |
| 5 | Kinase inhibition in rheumatoid arthritis: a big advance?显示文摘 | Pierre Miossec | 2013 | The Lancet2013，，9865： | 1 |
| 6 | IL-17 in rheumatoid arthritis:a new target for treatment or just another cytokine显示文摘 | Pierre Miossec | 2004 | Joint Bone Spine2004，71，2： | 1 |
| 7 | Th1/Th0 Cells but not by Th2 ceils IL-17 is produced by some pro-inflammatory 显示文摘 | Tanja Aarvak Martine Chabaud Pierre Miossec | 1999 | The Journal of hnmunology1999，162，3： | 1 |
| 8 | IL-17 and Th17 cells in human inflammatory diseases显示文摘 | Pierre Miossec | 2009 | Microbes and Infection2009，，5： | 1 |
| 9 | Bone marrow–derived and synovium‐derived mesenchymal cells promote Th17 cell expansion and activation through caspase 1 activation: Contribution to the chronicity of rheumatoid arthritis显示文摘 | Assia Eljaafari Marie‐Laure Tartelin Hanaa Aissaoui Guillaume Chevrel Bilal Osta Fabien Lavocat Pierre Miossec | 2012 | Arthritis & Rheumatism2012，，7： | 1 |
| 10 | Thl/Th0 Cells But Not by Th2 Cells IL - 17 Is Produced by Some Pro - inflam- matory显示文摘 | Tanja Aarvak Martine Chabaud Pierre Miossec | 1999 | The Journal of Immunology1999，162，： | 1 |
| 11 | mRNA Quantification of T-bet, GATA-3, IFN-γ, and IL-4 Shows a Defective Th1 Immune Response in the Peripheral Blood from Rheumatoid Arthritis Patients: Link with Disease Activity显示文摘 | Masanori Kawashima Pierre Miossec | 2005 | Journal of Clinical Immunology2005，，3： | 1 |
| 12 | IL-17 in rheumatoid arthritis:a new target for treatment or just another cytokine?显示文摘 | Pierre Miossec | 2004 | Joint Bone Spine2004，71，2： | 1 |
| 13 | lL-17 and Th17 cells in human inflammatory disea- ses 显示文摘 | Pierre Miossec | 2009 | Microbes and Infection2009，11，62： | 1 |
| 14 | Reactivation of latent tuberculosis with TNF inhibitors: critical role of the beta 2 chain of the IL-12 receptor显示文摘Tumor necrosis factor(TNF)inhibitors have improved a lot the treatment of numerous diseases,with the well-known example of rheumatoid arthritis(RA).In the early 2000s,postmarketing data quickly revealed an alarming number of severe tuberculosis(TB)under such treatment.These findings were consistent with previous results in mice where TNF is essential for lymph node formation and granuloma organization.The effects of TNF inhibition on RA synovium structure are very similar to those on granuloma,with changes in cellular interactions,cytokine,and chemokine production.In addition to the role of TNF in granuloma,the interleukin(IL)-12/interferon(IFN)-γpathway is required for an efficient host defense against TB.Primary and secondary immunodeficiencies affecting this pathway lead to severe bacillus Calmette-Guérin(BCG)reaction or full TB.Any chronic inflammation as in RA induces a systemic Th1 defect that predisposes to TB through specific downregulation of the IL-12Rß2 chain.When TNF inhibitors are initiated,this transiently increases this risk of TB,through effects on cellular interactions in a latent TB granuloma.At a later stage,when a better control disease activity is obtained,the risk of TB is reduced but not abrogated.Given the clear benefit from TNF inhibition,latent TB infection screening at baseline is essential for an optimal safety. | Marie Robert Pierre Miossec | 2021 | Cellular & Molecular Immunology2021，18，7： | 0 |
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