A tumor necrosis factor-α-inducible promoter variant of interferon-γ accelerates CD4+ T cell depletion in human immunodeficiency virus-1-infected individuals

被引：28

作者：

An, P

Vlahov, D

Margolick, JB

Phair, J

O'Brien, TR

Lautenberger, J

O'Brien, SJ

Winkler, CA

机构：

[1] NCI, Frederick Canc Res & Dev Ctr, Basic Res Program, SAIC Frederick Inc, Frederick, MD 21702 USA

[2] NCI, Lab Genom Divers, Frederick, MD 21702 USA

[3] Johns Hopkins Bloomberg Sch Publ Hlth, Baltimore, MD USA

[4] NCI, Viral Epidemiol Branch, DCEG, Bethesda, MD 20892 USA

[5] Northwestern Univ, Sch Med, Comprehens AIDS Ctr, Chicago, IL USA

来源：

JOURNAL OF INFECTIOUS DISEASES | 2003年 / 188卷 / 02期

关键词：

D O I：

10.1086/376455

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

A polymorphism, - 179G/T, in the promoter of the interferon (IFN)-gamma gene (IFNG) confers differential tumor necrosis factor-alpha (TNF-alpha) inducibility to the IFNG promoter. The rarer allele, -179T, but not -179G, is inducible by TNF-alpha. We investigated the effects of IFNG - 179G/T on AIDS pathogenesis. In 298 African American human immunodeficiency virus (HIV)-1 seroconverters, the IFNG - 179G/T genotype was associated with accelerated progression to CD4 < 200 and AIDS-1993, a finding suggesting that IFNG - 179T is a risk factor for AIDS progression, as measured by CD4 cell count. It is possible that increased IFN-γ production induced by TNF-α when - 179T is present causes CD4 cell depletion by apoptosis.

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页码：228 / 231

页数：4

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