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超抗原葡萄球菌肠毒素A诱导人单核细胞产生白细胞介素-1需要T细胞参与。

Induction of interleukin-1 in human monocytes by the superantigen staphylococcal enterotoxin A requires the participation of T cells.

作者信息

Gjörloff A, Fischer H, Hedlund G, Hansson J, Kenney J S, Allison A C, Sjögren H O, Dohlsten M

机构信息

Wallenberg Laboratory, Department of Tumor Immunology, University of Lund, Sweden.

出版信息

Cell Immunol. 1991 Oct 1;137(1):61-71. doi: 10.1016/0008-8749(91)90056-h.

DOI:10.1016/0008-8749(91)90056-h
PMID:1884398
Abstract

Nanogram quantities of the bacterial superantigen Staphylococcal Enterotoxin A (SEA) induced significant amounts of extracellular IL-1 alpha and IL-1 beta in human peripheral blood mononuclear cells. Induction of maximal IL-1 alpha and IL-1 beta levels by lipopolysaccharide (LPS) required microgram quantities. LPS induced detectable extracellular IL-1 content within 3-6 hr and maximal levels were detected already after 12 hr. Induction of IL-1 production by SEA showed a delayed release with peak values after 24-48 hr. IL-1 beta was the major species of IL-1 seen in both SEA- and LPS-stimulated culture supernatants. SEA was in general a relatively stronger inducer of extracellular IL-1 alpha than LPS. SEA-induced extracellular IL-1 production in human monocytes was entirely dependent on the presence of T cells, whereas addition of T cells to LPS-stimulated purified human monocytes only marginally enhanced the extracellular IL-1 production. The capacity to induce extracellular IL-1 production in monocytes in response to SEA was high in the CD4+ 45RO+ memory T cell subset, whereas CD4+ 45RA+ naive T cells and CD8+ T cells had lower IL-1-inducing capacity. The T cell help for IL-1 production could not be replaced by a panel of T cell-derived recombinant lymphokines added to SEA-stimulated monocytes, including IFN-gamma and TNF, indicating the participation of cell membrane-bound ligands or hitherto unidentified soluble mediators.

摘要

纳克量的细菌超抗原葡萄球菌肠毒素A(SEA)可诱导人外周血单核细胞产生大量细胞外白细胞介素-1α(IL-1α)和白细胞介素-1β(IL-1β)。脂多糖(LPS)诱导最大量的IL-1α和IL-1β水平需要微克量。LPS在3 - 6小时内诱导可检测到的细胞外IL-1含量,12小时后已检测到最大水平。SEA诱导IL-1产生表现为延迟释放,在24 - 48小时后达到峰值。IL-1β是在SEA和LPS刺激的培养上清液中所见IL-1的主要类型。总体而言,SEA比LPS是细胞外IL-1α相对更强的诱导剂。SEA诱导人单核细胞产生细胞外IL-1完全依赖于T细胞的存在,而将T细胞添加到LPS刺激的纯化人单核细胞中仅略微增强细胞外IL-1的产生。CD4 + 45RO +记忆T细胞亚群响应SEA诱导单核细胞产生细胞外IL-1的能力较高,而CD4 + 45RA +幼稚T细胞和CD8 + T细胞的IL-1诱导能力较低。添加到SEA刺激的单核细胞中的一组T细胞衍生的重组淋巴因子,包括干扰素-γ(IFN-γ)和肿瘤坏死因子(TNF),不能替代T细胞对IL-1产生的辅助作用,这表明细胞膜结合配体或迄今未鉴定的可溶性介质参与其中。

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