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NZB/NZW F1小鼠中异常的多克隆B细胞活化。

Abnormal polyclonal B cell activation in NZB/NZW F1 mice.

作者信息

Cohen P L, Ziff M

出版信息

J Immunol. 1977 Oct;119(4):1534-7.

PMID:561128
Abstract

Spleen cells from autoimmune (10-mont-old) NZB/NZW (B/W) mice failed to generate appreciable numbers of antibody-forming cells (AFC) in vitro to TNP-substituted sheep erythrocytes in response to the polyclonal B cell activators (PBA), LPS and PPD, despite normal DNA synthetic responses to these agents and normal AFC responses to TNP-Ficoll. The failure to respond to PBA in old B/W mice was not due to suppressor T cells since anti-brain-associated-theta-treated spleen cells still failed to generate AFC in response to PBA. The defect was age-related since cells from young B/W mice generated vigorous AFC responses to PBA. It is suggested that the failure of the spleen cells of old B/W mice to generate AFC is a result of in vitro polyclonal B cell activation in the course of autoantibody formation.

摘要

来自自身免疫性(10月龄)NZB/NZW(B/W)小鼠的脾细胞,尽管对这些试剂有正常的DNA合成反应以及对TNP-菲可产生正常的抗体形成细胞(AFC)反应,但在体外对多克隆B细胞激活剂(PBA)、脂多糖(LPS)和结核菌素纯蛋白衍生物(PPD)刺激下的TNP替代绵羊红细胞未能产生可观数量的抗体形成细胞(AFC)。老年B/W小鼠对PBA无反应并非由于抑制性T细胞,因为用抗脑相关θ处理的脾细胞对PBA仍无法产生AFC。该缺陷与年龄相关,因为年轻B/W小鼠的细胞对PBA能产生强烈的AFC反应。提示老年B/W小鼠脾细胞无法产生AFC是自身抗体形成过程中体外多克隆B细胞激活的结果。

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