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在特异性抗体存在的情况下,人类小胶质细胞介导抗新型隐球菌活性。

Human microglia mediate anti-Cryptococcus neoformans activity in the presence of specific antibody.

作者信息

Lee S C, Kress Y, Dickson D W, Casadevall A

机构信息

Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461, USA.

出版信息

J Neuroimmunol. 1995 Oct;62(1):43-52. doi: 10.1016/0165-5728(95)00097-l.

DOI:10.1016/0165-5728(95)00097-l
PMID:7499491
Abstract

The interaction of the opportunistic fungus Cryptococcus neoformans with human microglia was studied in vitro in the presence and absence of capsule binding antibody. In the absence of capsule binding antibody there was little or no phagocytosis. Addition of the murine monoclonal antibody (mAb) 2H1 (IgG1, kappa) to the capsular glucuronoxylomannan (GXM) produced a dose-dependent enhancement of C. neoformans phagocytosis by microglia. Phagocytosis resulted in marked inhibition of fungal proliferation. Microglial antifungal activity was studied by colony forming unit assay, L-[3H]leucine incorporation assay, and phase contrast microscopy. At microglia: C. neoformans ratios of 10:1 to 80:1 fungal growth was reduced by 61-95%. Inhibitors of nitric oxide synthase and reactive oxygen intermediates did not prevent antifungal activity mediated by human microglia. Transmission electron microscopic studies revealed that although some internalized yeast cells were killed, the majority were intact consistent with fungistasis. Human microglia cells are potent effector cells against C. neoformans in vitro in the presence of specific antibody. Enhancement of microglial activity in vivo by opsonins may be a useful therapeutic strategy.

摘要

在有或没有荚膜结合抗体的情况下,对机会性真菌新型隐球菌与人小胶质细胞的相互作用进行了体外研究。在没有荚膜结合抗体的情况下,几乎没有或不存在吞噬作用。向荚膜葡糖醛酸木聚糖(GXM)中添加鼠单克隆抗体(mAb)2H1(IgG1,κ)会导致小胶质细胞对新型隐球菌的吞噬作用呈剂量依赖性增强。吞噬作用导致真菌增殖受到显著抑制。通过菌落形成单位测定、L-[3H]亮氨酸掺入测定和相差显微镜对小胶质细胞的抗真菌活性进行了研究。在小胶质细胞与新型隐球菌比例为10:1至80:1时,真菌生长减少了61 - 95%。一氧化氮合酶抑制剂和活性氧中间体并不能阻止人小胶质细胞介导的抗真菌活性。透射电子显微镜研究表明,虽然一些内化的酵母细胞被杀死,但大多数细胞完整,这与抑菌作用一致。在特异性抗体存在的情况下,人小胶质细胞在体外是对抗新型隐球菌的有效效应细胞。调理素在体内增强小胶质细胞活性可能是一种有用的治疗策略。

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