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可增强由树突状细胞引发的混合淋巴细胞反应的巨噬细胞因子。

Macrophage factors which enhance the mixed leukocyte reaction initiated by dendritic cells.

作者信息

Naito K, Inaba K, Hirayama Y, Inaba-Miyama M, Sudo T, Muramatsu S

机构信息

Department of Zoology, Faculty of Science, Kyoto University, Japan.

出版信息

J Immunol. 1989 Mar 15;142(6):1834-9.

PMID:2522129
Abstract

Stimulator cells for the allogeneic MLR are dendritic cells but not macrophages (M phi). M phi, however, enhance the MLR initiated by relatively low doses of dendritic cells. The present report demonstrates that the enhancement of the MLR is mediated by two factors produced by M phi. One is IL-1, inasmuch as it has a Mr approximately 15 kDa, and both partially purified IL-1 and rIL-1 also enhance the MLR. The other has been identified as granulocyte-macrophage (GM)-CSF. It had a Mr approximately 25 kDa, and is reproduced by rGM-CSF. Moreover, the MLR-enhancing activity of both the 25-kDa molecule and rGM-CSF have been neutralized by anti-GM-CSF antiserum. Both IL-1 and GM-CSF have autonomous enhancing activity, but they collaborate with each other in enhancing the MLR. Both factors act on DC to augment their stimulatory activity for allogeneic T lymphocytes.

摘要

同种异体混合淋巴细胞反应(MLR)的刺激细胞是树突状细胞而非巨噬细胞(M phi)。然而,M phi可增强由相对低剂量树突状细胞引发的MLR。本报告表明,MLR的增强是由M phi产生的两种因子介导的。一种是白细胞介素-1(IL-1),因为其分子量约为15 kDa,部分纯化的IL-1和重组IL-1(rIL-1)也能增强MLR。另一种已被鉴定为粒细胞-巨噬细胞集落刺激因子(GM-CSF)。它的分子量约为25 kDa,重组GM-CSF(rGM-CSF)可重现其作用。此外,抗GM-CSF抗血清已中和了25 kDa分子和rGM-CSF的MLR增强活性。IL-1和GM-CSF都具有自主增强活性,但它们在增强MLR方面相互协作。这两种因子都作用于树突状细胞(DC),以增强其对同种异体T淋巴细胞的刺激活性。

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