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静止期系统性红斑狼疮患者体内人类T淋巴细胞表面分子的流动性受损。与cAMP信号通路缺陷的关系。

Impaired mobility of human T lymphocyte surface molecules during inactive systemic lupus erythematosus. Relationship to a defective cAMP pathway.

作者信息

Kammer G M, Mitchell E

机构信息

Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, Ohio.

出版信息

Arthritis Rheum. 1988 Jan;31(1):88-98. doi: 10.1002/art.1780310113.

Abstract

The T lymphocytes of patients with active systemic lupus erythematosus (SLE) exhibit impaired capping of the surface molecules CD3, CD4, and CD8 and a defective cAMP-dependent pathway. Since the mobility of these molecules is regulated in part by cAMP, we sought to determine whether there is a specific defect(s) along the T cell cAMP pathway that contributes to the persistent capping disorder observed during inactive SLE. The data suggest that a defect may exist at the level of cAMP-dependent protein kinase activation or at a point distally. We propose that a disorder of cAMP-dependent protein kinase activity might account for the defect of capping observed in both the CD3, CD4 (helper/inducer) and CD3, CD8 (suppressor) subsets observed in SLE.

摘要

活动性系统性红斑狼疮(SLE)患者的T淋巴细胞表现出表面分子CD3、CD4和CD8的帽化受损以及cAMP依赖性途径缺陷。由于这些分子的流动性部分受cAMP调节,我们试图确定T细胞cAMP途径中是否存在特定缺陷,该缺陷导致在非活动性SLE期间观察到的持续性帽化障碍。数据表明,缺陷可能存在于cAMP依赖性蛋白激酶激活水平或更远端的位点。我们提出,cAMP依赖性蛋白激酶活性紊乱可能解释了在SLE中观察到的CD3、CD4(辅助/诱导)和CD3、CD8(抑制)亚群中帽化缺陷。

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