CD20+ B 细胞耗竭在系统性自身免疫性疾病中的作用：抑制的共同机制还是对体液免疫的疾病特异性影响？
CD20+ B cell depletion in systemic autoimmune diseases: common mechanism of inhibition or disease-specific effect on humoral immunity?
机构信息
Department of Renal Medicine, Papageorgiou Hospital, 56403 Thessaloniki, Greece.
2nd Prop Department of Internal Medicine, Hippokration General Hospital, Konstantinoupoleos 49, 54642 Thessaloniki, Greece.
出版信息
Biomed Res Int. 2014;2014:973609. doi: 10.1155/2014/973609. Epub 2014 Mar 27.
Abstract
Autoimmunity remains a complex physiologic deviation, enabled and perpetuated by a variety of interplayers and pathways. Simplistic approaches, targeting either isolated end-effectors of more centrally placed interactors of these mechanisms, are continuously tried in an effort to comprehend and halt cascades with potential disabling and deleterious effects in the affected individuals. This review focuses on theoretical and clinically proved effects of rituximab-induced CD20+ B cell depletion on different systemic autoimmune diseases and extrapolates on pathogenetic mechanisms that may account for different interindividual or interdisease responses.
摘要
自身免疫仍然是一种复杂的生理偏差，由多种相互作用和途径所导致和维持。人们一直在尝试采用简化方法，针对这些机制的更中心相互作用的孤立末端效应器，以努力理解和阻止潜在的致残和有害影响的级联反应。这篇综述重点介绍了利妥昔单抗诱导的 CD20+ B 细胞耗竭对不同系统性自身免疫性疾病的理论和临床证实的影响，并推断了可能导致不同个体间或疾病间反应的发病机制。
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