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巨噬细胞抑制T细胞介导的淋巴因子产生,但不抑制细胞毒性活性。

Suppression of T-cell mediated lymphokine production but not cytotoxic activity by macrophages.

作者信息

Varesio L, Eva A, Cavallo G, Herberman R B

出版信息

Boll Ist Sieroter Milan. 1980 Mar 31;59(1):12-6.

PMID:6970038
Abstract

We directly compared the effects of macrophages from infiltrating MSV-induced regressing tumors (T-M0) or from the peritoneal cavity of mice previously injected with light mineral oil (LMO-M0) on two functions of alloimmune spleen cells (ISC), the cytotoxic activity and production of a lymphokine, macrophage inhibitory factor (MIF). Addition of T-M0 or LMO-M0 to ISC did not inhibit their cytotoxicity. In contrast, T-M0, but not LMO-M0, mixed with ISC inhibited their ability to produce MIF. We propose that the differential sensitivity of the two immune functions to the macrophage-dependent suppressor activity is due to the ability to M0 to inhibit lymphocyte protein synthesis, with MIF production, but not T cell killing, requiring active protein synthesis.

摘要

我们直接比较了来自浸润性MSV诱导的消退肿瘤(T-M0)或先前注射轻质矿物油的小鼠腹腔(LMO-M0)的巨噬细胞对同种异体免疫脾细胞(ISC)的两种功能的影响,即细胞毒性活性和淋巴因子巨噬细胞抑制因子(MIF)的产生。将T-M0或LMO-M0添加到ISC中不会抑制它们的细胞毒性。相反,与ISC混合的T-M0而非LMO-M0会抑制它们产生MIF的能力。我们提出,这两种免疫功能对巨噬细胞依赖性抑制活性的不同敏感性是由于M0抑制淋巴细胞蛋白质合成的能力,其中MIF的产生需要活跃的蛋白质合成,但T细胞杀伤则不需要。

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