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新型隐球菌的甘露糖蛋白可诱导人外周血单个核细胞(PBMC)产生增殖反应,并增强HIV-1复制。

Mannoproteins of Cryptococcus neoformans induce proliferative response in human peripheral blood mononuclear cells (PBMC) and enhance HIV-1 replication.

作者信息

Orendi J M, Verheul A F, De Vos N M, Visser M R, Snippe H, Cherniak R, Vaishnav V V, Rijkers G T, Verhoef J

机构信息

Eijkman-Winkler Institute for Microbiology, Infectious Diseases, and Inflammation, University Hospital, Utrecht, The Netherlands.

出版信息

Clin Exp Immunol. 1997 Feb;107(2):293-9. doi: 10.1111/j.1365-2249.1997.283-ce1169.x.

DOI:10.1111/j.1365-2249.1997.283-ce1169.x
PMID:9030866
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1904591/
Abstract

To investigate the possible role of Cryptococcus neoformans var. neoformans in HIV disease progression, and to identify the responsible cryptococcal components, an in vitro cell culture model was set up to study the C. neoformans-induced enhancement of HIV replication in HIV-1-infected PBMC. Similar to whole C. neoformans, cell-wall membrane fraction and mannoproteins induced proliferation of PBMC and enhancement of lymphotropic HIV replication in HIV-infected PBMC, while galactoxylomannan did not. MoAbs capable of interfering with MHC class II-mediated antigen presentation prevented the induction of cell proliferation by whole C. neoformans or cryptococcal mannoproteins. MoAb binding to adhesion molecules intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) also inhibited C. neoformans-induced cell proliferation. In addition, anti-MHC class II MoAb inhibited the enhancement of HIV replication by C. neoformans. The results suggest that: (i) C. neoformans may accelerate HIV disease progression by stimulation of HIV replication through MHC class II-mediated antigen presentation; and (ii) cryptococcal mannoprotein may be one of the responsible components. The ability to enhance HIV replication in PBMC in vitro is not unique for C. neoformans. However, this is the first report to study in detail a yeast-induced enhancement of HIV replication in PBMC.

摘要

为了研究新型隐球菌新型变种在HIV疾病进展中的可能作用,并确定相关的隐球菌成分,建立了一种体外细胞培养模型,以研究新型隐球菌诱导HIV-1感染的外周血单个核细胞(PBMC)中HIV复制增强的情况。与完整的新型隐球菌相似,细胞壁膜组分和甘露糖蛋白可诱导PBMC增殖,并增强HIV感染的PBMC中嗜淋巴细胞性HIV的复制,而半乳甘露聚糖则无此作用。能够干扰MHC II类分子介导的抗原呈递的单克隆抗体(MoAb)可阻止完整的新型隐球菌或隐球菌甘露糖蛋白诱导细胞增殖。与黏附分子细胞间黏附分子-1(ICAM-1)和淋巴细胞功能相关抗原-1(LFA-1)结合的MoAb也可抑制新型隐球菌诱导的细胞增殖。此外,抗MHC II类MoAb可抑制新型隐球菌对HIV复制的增强作用。结果表明:(i)新型隐球菌可能通过MHC II类分子介导的抗原呈递刺激HIV复制,从而加速HIV疾病进展;(ii)隐球菌甘露糖蛋白可能是相关成分之一。体外增强PBMC中HIV复制的能力并非新型隐球菌所特有。然而,这是首次详细研究酵母诱导PBMC中HIV复制增强的报告。

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