期刊
AUTOIMMUNITY REVIEWS
卷 7, 期 2, 页码 149-154出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.autrev.2007.02.016
关键词
systemic lupus erythematosus; B lymphocyte; CD5; chronic lymphocytic leukemia
类别
The pathophysiological relevance of B cells for systemic lupus erythematosus (SLE), particularly those expressing the T-cell marker CD5, raises the question as to how they operate upon autoimmune processes. Based on their production of low-affinity multispecific antibodies (Abs), CD5(+) B lymphocytes, also referred to as B1 cells, have originally been endowed with the autoAb making. It has since been established that high-affinity Abs to double-stranded DNA are not generated by these cells, but rather by B2 cells. It does not appear that they have the exclusive rights to the production of pathogenic autoAbs. In the light of recent findings, CD5 plays a paradoxical role in preventing autoimmunity. Hence, misguided signaling through CD5 could lead to autoimmunity. This provocative view differs from the naive interpretation that the increased levels of B1 cells in SLE represent a direct source of autoAbs responsible for damaging organs. (C) 2007 Elsevier B.V. All rights reserved.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据