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前列腺素E2可抑制佛波酯加钙离子载体激活的小鼠T细胞克隆的增殖,但不抑制其白细胞介素-2的产生。

Prostaglandin E2 inhibits proliferation but not interleukin-2 production by phorbol ester plus calcium ionophore-activated murine T cell clones.

作者信息

Cunha-Neto E, Rizzo L V

机构信息

Departamento de Medicina Complementar, Faculdade de Ciências da Saúde, Universidade de Brasília, Brasil.

出版信息

Braz J Med Biol Res. 1989;22(3):365-77.

PMID:2804471
Abstract
  1. We have investigated the effect of prostaglandin E2 (PGE2) on the T lymphocyte activation pathway. 2. At physiologically attainable concentrations (approximately 0.1 microM), PGE2 effectively inhibited the proliferation of murine antigen-specific "helper" T cell clones stimulated either with specific antigen in the presence of macrophages or with phorbol ester plus calcium ionophore A23187. The inhibition was not reversed by the addition of exogenous Interleukin 2 (IL-2) in either case. 3. PGE2 treatment at the same concentrations did not inhibit IL-2 production by phorbol ester plus calcium ionophore-stimulated T cell clones as assayed by CTLL proliferation. 4. These results suggest that the major target (or targets) of PGE2 inhibition directly on T cells lies in the IL-2 signal transduction pathway rather than in the early activation events leading to T cell activation.
摘要
  1. 我们研究了前列腺素E2(PGE2)对T淋巴细胞激活途径的影响。2. 在生理可达到的浓度(约0.1微摩尔)下,PGE2有效抑制了小鼠抗原特异性“辅助”T细胞克隆的增殖,这些克隆在巨噬细胞存在下用特异性抗原刺激,或用佛波酯加钙离子载体A23187刺激。在这两种情况下,添加外源性白细胞介素2(IL-2)均不能逆转这种抑制作用。3. 用CTLL增殖法检测,相同浓度的PGE2处理并未抑制佛波酯加钙离子载体刺激的T细胞克隆产生IL-2。4. 这些结果表明,PGE2对T细胞的直接抑制作用的主要靶点在于IL-2信号转导途径,而非导致T细胞激活的早期激活事件。

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