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关节炎支原体来源的T细胞有丝分裂原的H2基因控制及生物学活性:综述

H2 gene control and biological activities of a T-cell mitogen derived from Mycoplasma arthritidis: a review.

作者信息

Cole B C

出版信息

Yale J Biol Med. 1983 Sep-Dec;56(5-6):605-12.

Abstract

Mycoplasma arthritidis generates a soluble, non-dialysable, polyclonal mitogen which is active for murine and human T lymphocytes in the presence of an adherent, radio-resistant, Ia-bearing accessory cell population. Genetic analysis has established that the I-E sub-region of the murine H2 gene complex controls responses to the mitogen and that this control is exercised at the level of the Ia-bearing accessory cell. Lymphocyte proliferation, induction of cytotoxic lymphocytes, and interferon induction are all under Ir gene control and appear to be dependent upon binding of the mitogen to a specific Ia antigen present on a subset of splenic cells. This mycoplasma mitogen provides a new model system to define the mechanisms of Ir gene control of lymphocyte activation.

摘要

关节炎支原体产生一种可溶的、不可透析的多克隆丝裂原,在存在贴壁的、抗辐射的、表达Ia的辅助细胞群体的情况下,该丝裂原对小鼠和人类T淋巴细胞具有活性。遗传分析表明,小鼠H2基因复合体的I-E亚区控制对该丝裂原的反应,并且这种控制是在表达Ia的辅助细胞水平上进行的。淋巴细胞增殖、细胞毒性淋巴细胞的诱导以及干扰素诱导均受Ir基因控制,并且似乎依赖于丝裂原与脾细胞亚群上存在的特定Ia抗原的结合。这种支原体丝裂原为定义Ir基因对淋巴细胞激活的控制机制提供了一个新的模型系统。

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