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逆转录病毒通过阻断树突状细胞迁移和下调黏附分子诱导免疫抑制。

Retrovirus-induced immunosuppression via blocking of dendritic cell migration and down-regulation of adhesion molecules.

作者信息

Gabrilovich D I, Woods G M, Patterson S, Harvey J J, Knight S C

机构信息

Antigen Presentation Research Group, Clinical Research Centre, Harrow, U.K.

出版信息

Immunology. 1994 May;82(1):82-7.

Abstract

Dendritic cells (DC) within tissues may acquire and process antigens, carry them into lymph nodes and cluster and activate T cells. The ability of DC to acquire antigen and to migrate to lymph nodes was estimated during murine retroviral infection caused by Rauscher leukaemia virus (RLV). A novel mechanism of inducing immunodeficiency has now been identified. In mice infected with RLV, DC failed to migrate into lymph nodes following exposure of the skin to the contact sensitizer, fluorescein isothiocyanate. RLV infection of a proportion of DC both in skin and lymph nodes, shown by semi-quantitative polymerase chain reaction (PCR) and down-regulation of expression of adhesion molecules (CD54 and CD44) on the surface of Langerhans' cells, may contribute to the described phenomenon. A failure of DC migration could be an important immunosuppressive mechanism of RLV infection in mice and we speculate on a similar role for DC in human immunodeficiency virus-1 (HIV-1) infection in humans.

摘要

组织中的树突状细胞(DC)可以获取并处理抗原,将其带入淋巴结并聚集和激活T细胞。在由劳舍尔白血病病毒(RLV)引起的小鼠逆转录病毒感染期间,评估了DC获取抗原并迁移至淋巴结的能力。现已确定了一种诱导免疫缺陷的新机制。在用RLV感染的小鼠中,皮肤接触接触性致敏剂异硫氰酸荧光素后,DC无法迁移至淋巴结。半定量聚合酶链反应(PCR)显示,皮肤和淋巴结中的一部分DC受到RLV感染,且朗格汉斯细胞表面的黏附分子(CD54和CD44)表达下调,这可能导致了上述现象。DC迁移失败可能是RLV感染小鼠的一种重要免疫抑制机制,我们推测DC在人类免疫缺陷病毒1型(HIV-1)感染人类中也发挥类似作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c4ba/1414836/e20d2dd9e100/immunology00080-0087-a.jpg

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