人类CD4分子在神经退行性变中的新作用被发现。

Novel role of human CD4 molecule identified in neurodegeneration.

作者信息

Buttini M, Westland C E, Masliah E, Yafeh A M, Wyss-Coray T, Mucke L

机构信息

Department of Neurology, University of California, San Francisco 94141-9100, USA.

出版信息

Nat Med. 1998 Apr;4(4):441-6. doi: 10.1038/nm0498-441.

DOI:10.1038/nm0498-441

PMID:9546790

Abstract

The human CD4 molecule (hCD4) is expressed on T lymphocytes and macrophages and acts as a key component of the cellular receptor for HIV. At baseline, hCD4 transgenic mice expressed hCD4 on microglia, the resident mononuclear phagocytes of the brain, and showed no neuronal damage. Activation of brain microglia by peripheral immune challenges elicited neurodegeneration in hCD4 mice but not in nontransgenic controls. In post-mortem brain tissues from AIDS patients with opportunistic infections, but without typical HIV encephalitis, hCD4 expression correlated with neurodegeneration. We conclude that hCD4 may function as an important mediator of indirect neuronal damage in infectious and immune-mediated diseases of the central nervous system.

摘要

人类CD4分子（hCD4）在T淋巴细胞和巨噬细胞上表达，是HIV细胞受体的关键组成部分。在基线时，hCD4转基因小鼠在小胶质细胞（大脑中的常驻单核吞噬细胞）上表达hCD4，且未显示出神经元损伤。外周免疫刺激激活脑小胶质细胞会引发hCD4小鼠的神经退行性变，但在非转基因对照小鼠中则不会。在患有机会性感染但无典型HIV脑炎的艾滋病患者的尸检脑组织中，hCD4表达与神经退行性变相关。我们得出结论，hCD4可能是中枢神经系统感染性和免疫介导性疾病中间接神经元损伤的重要介质。