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新型隐球菌激活骨髓来源的传统树突状细胞而非浆细胞样树突状细胞,并下调巨噬细胞。

Cryptococcus neoformans activates bone marrow-derived conventional dendritic cells rather than plasmacytoid dendritic cells and down-regulates macrophages.

作者信息

Siegemund Sabine, Alber Gottfried

机构信息

Institute of Immunology, College of Veterinary Medicine, Leipzig, Germany.

出版信息

FEMS Immunol Med Microbiol. 2008 Apr;52(3):417-27. doi: 10.1111/j.1574-695X.2008.00391.x.

Abstract

Induction of IL-12 and IL-23 is essential for protective immunity against Cryptococcusneoformans. The contribution of dendritic cells vs. macrophages to IL-12/23 production in response to C. neoformans infection is unclear. Activation of conventional bone marrow-derived dendritic cells (BMDC), plasmacytoid BMDC, and bone marrow-derived macrophages (BMMPhi) was assessed by analyzing cytokine responses and the expression of MHC-II, CD86, and CD80 in each cell type. Cryptococcus neoformans induced the release of IL-12/23p40 by BMDC, but not by BMMPhi, in a TLR2- and TLR4-independent but MyD88-dependent manner. Conventional BMDC rather than plasmacytoid BMDC up-regulated MHC-II and CD86, while BMMPhi down-regulated MHC-II and CD86 in response to C. neoformans. The up-regulation of MHC-II and CD86 on BMDC required MyD88. Our data point to conventional DC as critical IL-12/23-producing antigen-presenting cells during cryptococcosis.

摘要

诱导IL-12和IL-23对于针对新型隐球菌的保护性免疫至关重要。在新型隐球菌感染后,树突状细胞与巨噬细胞对IL-12/23产生的贡献尚不清楚。通过分析细胞因子反应以及每种细胞类型中MHC-II、CD86和CD80的表达,评估了传统骨髓来源的树突状细胞(BMDC)、浆细胞样BMDC和骨髓来源的巨噬细胞(BMMPhi)的活化情况。新型隐球菌以不依赖TLR2和TLR4但依赖MyD88的方式诱导BMDC释放IL-12/23p40,而BMMPhi则不释放。传统BMDC而非浆细胞样BMDC上调MHC-II和CD86,而BMMPhi在新型隐球菌刺激下下调MHC-II和CD86。BMDC上MHC-II和CD86的上调需要MyD88。我们的数据表明,在隐球菌病期间,传统DC是产生关键IL-12/23的抗原呈递细胞。

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