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纤维肉瘤衍生的转化生长因子-β1诱导巨噬细胞抑制活性：对静息巨噬细胞和活化巨噬细胞的不同影响。

Induction of macrophage suppressor activity by fibrosarcoma-derived transforming growth factor-beta 1: contrasting effects on resting and activated macrophages.

作者信息

Alleva D G, Walker T M, Elgert K D

机构信息

Department of Biology, Virginia Polytechnic Institute and State University, Blacksburg 24061-0406, USA.

出版信息

J Leukoc Biol. 1995 Jun;57(6):919-28. doi: 10.1002/jlb.57.6.919.

DOI:10.1002/jlb.57.6.919
PMID:7790775
Abstract

Tumor-derived transforming growth factor-beta 1 (TGF-beta 1) suppresses several immune responses. Because tumor growth induces macrophage (m phi) suppressor activity, we determined whether murine fibrosarcoma-derived TGF-beta 1 contributed to m phi-mediated suppression of autoantigen- and alloantigen-stimulated T cell proliferation. The murine fibrosarcoma Meth-KDE cell line constitutively produced TGF-beta 1. Meth-KDE tumor-bearing host (TBH) syngeneic splenic m phi s suppressed autoantigen- and alloantigen-stimulated normal host (NH) CD4+ T cell proliferation. Pretreatment with Meth-KDE supernatants induced NH m phi s to suppress T cell proliferation as much as TBH m phi s. Anti-TGF-beta 1 antibody treatment reversed Meth-KDE-induced NH m phi-mediated suppression. Recombinant TGF-beta 1-induced m phi-mediated suppression was not blocked during inhibition of prostaglandin E2 (PGE2), nitric oxide (NO), or TGF-beta 1 production. However, Meth-KDE-induced m phi-mediated suppression was partly reduced when PGE2 production was inhibited. Pretreatment with tumor cell-derived TGF-beta 1, but not recombinant TGF-beta 1, increased activated m phi PGE2 production. These results show that additional tumor-derived molecules aid in TGF-beta 1-enhanced PGE2 production. Also, TGF-beta 1 alone up-regulates m phi synthesis of suppressor molecules that are different from PGE2, NO, and TGF-beta 1. Although TGF-beta 1 has direct suppressor activity on lymphocytes, these results show that release of tumor cell TGF-beta 1 also induces m phi suppressor activity.

摘要

肿瘤来源的转化生长因子-β1（TGF-β1）可抑制多种免疫反应。由于肿瘤生长会诱导巨噬细胞（m phi）产生抑制活性，我们研究了小鼠纤维肉瘤来源的TGF-β1是否有助于m phi介导的对自身抗原和同种异体抗原刺激的T细胞增殖的抑制作用。小鼠纤维肉瘤Meth-KDE细胞系可组成性产生TGF-β1。携带Meth-KDE肿瘤的宿主（TBH）同基因脾m phi可抑制自身抗原和同种异体抗原刺激的正常宿主（NH）CD4 + T细胞增殖。用Meth-KDE上清液预处理可诱导NH m phi抑制T细胞增殖，其抑制程度与TBH m phi相同。抗TGF-β1抗体处理可逆转Meth-KDE诱导的NH m phi介导的抑制作用。在抑制前列腺素E2（PGE2）、一氧化氮（NO）或TGF-β1产生的过程中，重组TGF-β1诱导的m phi介导的抑制作用未被阻断。然而，当PGE2产生受到抑制时，Meth-KDE诱导的m phi介导的抑制作用部分降低。用肿瘤细胞来源的TGF-β1预处理可增加活化的m phi的PGE2产生，但用重组TGF-β1预处理则无此作用。这些结果表明，肿瘤来源的其他分子有助于TGF-β1增强PGE2的产生。此外，单独的TGF-β1可上调m phi中不同于PGE2、NO和TGF-β1的抑制分子的合成。尽管TGF-β1对淋巴细胞具有直接抑制活性，但这些结果表明肿瘤细胞TGF-β1的释放也可诱导m phi抑制活性。

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