AN HIV-1-INFECTED T-CELL CLONE DEFECTIVE IN IL-2 PRODUCTION AND CA2+ MOBILIZATION AFTER CD3 STIMULATION

被引：0

作者：

PEREZ, VL

ROWE, T

JUSTEMENT, JS

BUTERA, ST

JUNE, CH

FOLKS, TM

机构：

[1] CTR DIS CONTROL, CTR INFECT DIS, DIV VIRAL & RICKETTSIAL DIS, RETROVIRUS DIS BRANCH, ATLANTA, GA 30333 USA

[2] NATL NAVAL MED CTR, NAVAL MED RES INST, BETHESDA, MD 20892 USA

[3] NIAID, IMMUNOREGULAT LAB, BETHESDA, MD 20892 USA

来源：

JOURNAL OF IMMUNOLOGY | 1991年 / 147卷 / 09期

关键词：

D O I：

暂无

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 chronically HIV-1-infected T cell clone (J1.1) derived from Jurkat cells was developed that possesses defects in CD3 signaling. This clone was phenotypically determined to be CD4- and express a reduced surface density of CD3 as compared with a pool of uninfected Jurkat clones. Although J1.1 could be induced with TNF-alpha to produce HIV-1 particles, stimulation via the CD3 (T3-Ti) complex, using mAb cross-linking, had no effect on viral production. Further investigation revealed that J1.1 secreted approximately 20-fold less IL-2 than did uninfected Jurkat cells after anti-CD3 treatment. In addition, a separate defect in Ca2+ mobilization was noted in the HIV-1-infected J1.1 line when compared with uninfected Jurkat cells after anti-CD3 cross-linking. The cell line described offers a new model in which to study the mechanisms of several defects directly imposed by HIV-1 on CD3+ cells.

引用

页码：3145 / 3148

页数：4

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