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小鼠中 pristane 诱导的关节炎。III. pristane 诱导的关节炎发生之前淋巴细胞的表型和功能异常。

Pristane-induced arthritis in mice. III. Lymphocyte phenotypic and functional abnormalities precede the development of pristane-induced arthritis.

作者信息

Wooley P H, Whalen J D

机构信息

Department of Internal Medicine, Wayne State University Medical School, Detroit, Michigan 48202.

出版信息

Cell Immunol. 1991 Nov;138(1):251-9. doi: 10.1016/0008-8749(91)90150-a.

Abstract

Pristane injection caused mediastinal lymphadenopathy in arthritis-susceptible DBA/1 mice, but not in arthritis-resistant DBA/2 mice. Early DBA/1 mediastinal lymph node changes were characterized by the accumulation of surface Ig+ cells and a CD8+ (Lyt 2) lymphocyte population, causing an inversion of the CD4/CD8 ratio. Depressed mitogen responses and the appearance of a nonspecific suppressor cell population were coincidental with the CD8+ cell accumulation. Prior to the development of overt clinical arthritis, an expansion of CD4+ (L3T4) lymphocytes displaced CD8+ as the predominant phenotype in mediastinal node. Mitogen responses were restored and suppressor cell activity was abrogated concomitant with the expansion of the CD4+ cell population.

摘要

pristane注射在易患关节炎的DBA/1小鼠中引起纵隔淋巴结病,但在抗关节炎的DBA/2小鼠中未引起。早期DBA/1纵隔淋巴结变化的特征是表面Ig+细胞和CD8+(Lyt 2)淋巴细胞群的积累,导致CD4/CD8比值倒置。有丝分裂原反应降低和非特异性抑制细胞群的出现与CD8+细胞积累同时发生。在明显的临床关节炎发展之前,CD4+(L3T4)淋巴细胞的扩增取代CD8+成为纵隔淋巴结中的主要表型。有丝分裂原反应恢复,抑制细胞活性随着CD4+细胞群的扩增而消除。

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