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人类树突状细胞中白细胞介素12和白细胞介素23产生的差异调节

Differential regulation of interleukin 12 and interleukin 23 production in human dendritic cells.

作者信息

Gerosa Franca, Baldani-Guerra Barbara, Lyakh Lyudmila A, Batoni Giovanna, Esin Semih, Winkler-Pickett Robin T, Consolaro Maria Rita, De Marchi Mario, Giachino Daniela, Robbiano Angela, Astegiano Marco, Sambataro Angela, Kastelein Robert A, Carra Giuseppe, Trinchieri Giorgio

机构信息

Department of Pathology, Section of Immunology, University of Verona, 37134 Verona, Italy.

出版信息

J Exp Med. 2008 Jun 9;205(6):1447-61. doi: 10.1084/jem.20071450. Epub 2008 May 19.

Abstract

We analyzed interleukin (IL) 12 and IL-23 production by monocyte-derived dendritic cells (mono-DCs). Mycobacterium tuberculosis H37Rv and zymosan preferentially induced IL-23. IL-23 but not IL-12 was efficiently induced by the combination of nucleotide-binding oligodimerization domain and Toll-like receptor (TLR) 2 ligands, which mimics activation by M. tuberculosis, or by the human dectin-1 ligand beta-glucan alone or in combination with TLR2 ligands, mimicking induction by zymosan. TLR2 ligands inhibited IL-12 and increased IL-23 production. DC priming with interferon (IFN) gamma strongly increased IL-12 production, but was not required for IL-23 production and inhibited IL-23 production induced by beta-glucan. The pattern of IL-12 and IL-23 induction was reflected in accumulation of the IL-12p35 and IL-23p19 transcripts, respectively, but not IL-12/23p40. Although IL-23, transforming growth factor beta, and IL-6 contained in the supernatants of activated mono-DCs played a role in the induction of IL-17 by human CD4(+) T cells, IL-1beta, in combination with one or more of those factors, was required for IL-17 production, and its production determined the differential ability of the stimuli used to elicit mono-DCs to produce soluble factors directing IL-17 production. Thus, the differential ability of pathogens to induce antigen-presenting cells to produce cytokines regulates the immune response to infection.

摘要

我们分析了单核细胞衍生树突状细胞(单核细胞来源的树突状细胞)产生白细胞介素(IL)-12和IL-23的情况。结核分枝杆菌H37Rv和酵母聚糖优先诱导IL-23的产生。核苷酸结合寡聚化结构域与Toll样受体(TLR)2配体的组合可有效诱导IL-23而非IL-12的产生,该组合模拟了结核分枝杆菌的激活作用;单独的人源性树突状细胞相关C型凝集素-1配体β-葡聚糖或其与TLR2配体的组合也可诱导IL-23的产生,模拟了酵母聚糖的诱导作用。TLR2配体抑制IL-12的产生并增加IL-23的产生。用干扰素(IFN)γ预处理树突状细胞可强烈增加IL-12的产生,但IL-23的产生并不需要IFNγ,且IFNγ可抑制β-葡聚糖诱导的IL-23的产生。IL-12和IL-23诱导模式分别反映在IL-12p35和IL-23p19转录本的积累上,而非IL-12/23p40的积累上。尽管活化的单核细胞来源的树突状细胞上清液中所含的IL-23、转化生长因子β和IL-6在人CD4(+) T细胞诱导IL-17的过程中发挥了作用,但IL-1β与这些因子中的一种或多种共同作用是IL-17产生所必需的,并且IL-1β的产生决定了用于激发单核细胞来源的树突状细胞产生指导IL-17产生的可溶性因子的刺激物的差异能力。因此,病原体诱导抗原呈递细胞产生细胞因子的差异能力调节了对感染的免疫反应。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bf7c/2413040/91526f6cc543/jem2051447f01.jpg

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