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一只缺乏外周CD4淋巴细胞的非洲绿猴,其保留辅助性T细胞活性并与猴免疫缺陷病毒非洲绿猴株共存。

An African green monkey lacking peripheral CD4 lymphocytes that retains helper T cell activity and coexists with SIVagm.

作者信息

Murayama Y, Mukai R, Inoue-Murayama M, Yoshikawa Y

机构信息

National Institute of Animal Health, Kannondai, Tsukuba, Ibaraki.

出版信息

Clin Exp Immunol. 1999 Sep;117(3):504-12. doi: 10.1046/j.1365-2249.1999.00999.x.

Abstract

Natural infection with simian immunodeficiency virus (SIV) is known to occur in the African green monkey (AGM). The actual onset of the disease has not been recognized in SIVagm infected AGM, and the precise reason for such apathogenicity in the AGM remains unclear. We reported previously that AGM peripheral CD4 lymphocytes underwent a peculiar differentiation from CD4+ to CD4- cells after in vitro activation, and we inferred that the AGM does not fall into a fatal immunodeficient state because of the generation of CD4- helper T cells in vivo. To evaluate this possibility, we examined the relationship between CD4 expression and helper T cell activity in the naturally infected AGM. We identified a healthy monkey almost lacking CD4 T cells in the periphery. This AGM showed no signs and symptoms of immunodeficiency and retained a helper T cell activity in antibody production comparable to those of CD4+ AGMs. In addition, SIVagm could be isolated from CD8+ lymphocytes in the CD4- AGM. These observations suggest that a unique host-virus adaptation has developed in the AGM, and may be helpful in explaining the fundamental reason for the apathogenicity occurring in this monkey.

摘要

已知非洲绿猴(AGM)会自然感染猴免疫缺陷病毒(SIV)。在感染SIVagm的AGM中尚未发现该疾病的实际发病情况,并且AGM中这种无致病性的确切原因仍不清楚。我们之前报道过,AGM外周血CD4淋巴细胞在体外激活后会经历从CD4 +细胞到CD4 -细胞的特殊分化,并且我们推测AGM不会因体内产生CD4 -辅助性T细胞而陷入致命的免疫缺陷状态。为了评估这种可能性,我们研究了自然感染的AGM中CD4表达与辅助性T细胞活性之间的关系。我们鉴定出一只外周几乎缺乏CD4 T细胞的健康猴子。这只AGM没有免疫缺陷的迹象和症状,并且在抗体产生方面保留了与CD4 + AGM相当的辅助性T细胞活性。此外,在CD4 -的AGM中,可以从CD8 +淋巴细胞中分离出SIVagm。这些观察结果表明,AGM中已经形成了独特的宿主 - 病毒适应性,这可能有助于解释这种猴子发生无致病性的根本原因。

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