Eisenberg R A, Sobel E S, Reap E A, Halpern M D, Cohen P L
Department of Medicine, University of North Carolina at Chapel Hill 27599-7280.
Semin Immunol. 1994 Feb;6(1):49-54. doi: 10.1006/smim.1994.1008.
B cell abnormalities play a central role in the systemic autoimmune syndromes of lpr and gld mice. In the lpr model, autoantibody production requires the intrinsic expression of the lpr gene in B cells, while in the gld mouse the genetic defect is extrinsic, yet probably results in a similar failure of B cell tolerance. Despite their abnormality, lpr B cells require lpr (abnormal) T cells in order to produce autoantibodies.
B细胞异常在lpr和gld小鼠的系统性自身免疫综合征中起核心作用。在lpr模型中,自身抗体的产生需要B细胞中lpr基因的内在表达,而在gld小鼠中,基因缺陷是外在的,但可能导致类似的B细胞耐受性缺失。尽管lpr B细胞存在异常,但为了产生自身抗体,它们需要lpr(异常)T细胞。