Anolik Jennifer, Sanz Iñaki
Department of Medicine, Clinical Immunology and Rheumatology Unit, Rochester, New York 14642, USA.
Curr Opin Rheumatol. 2004 Sep;16(5):505-12. doi: 10.1097/01.bor.0000133660.52599.f6.
The purpose of this review is to discuss recent publications dealing with the control of autoreactive B cells, how this control is subverted in human systemic lupus erythematosus and in murine models of systemic lupus erythematosus, and how dysregulated autoreactive B cells may then contribute to disease expression through both regulatory and effector mechanisms.
Autoreactive B cells are abundant in the mature peripheral B-cell repertoire and need to be censored to avoid autoimmunity. This censoring is accomplished in diverse ways and may be broken down by multiple mechanisms both intrinsic and extrinsic to the B cells.
The work reviewed here paints a suggestive picture while confirming the pathogenic potential of autoreactive B cells and pointing to specific defects that warrant further exploration and could represent future therapeutic targets for this autoimmune disease.
本综述旨在讨论近期关于自身反应性B细胞控制的出版物，这种控制在人类系统性红斑狼疮和系统性红斑狼疮小鼠模型中是如何被破坏的，以及失调的自身反应性B细胞如何通过调节和效应机制导致疾病表现。
自身反应性B细胞在成熟外周B细胞库中大量存在，需要进行审查以避免自身免疫。这种审查通过多种方式完成，并且可能被B细胞内在和外在的多种机制破坏。
本文所综述的研究描绘了一幅具有启发性的图景，同时证实了自身反应性B细胞的致病潜力，并指出了一些特定缺陷，这些缺陷值得进一步探索，可能代表这种自身免疫性疾病未来的治疗靶点。
