J Immunol. 1991 Nov 1;147(9):3145-8.

An HIV-1-infected T cell clone defective in IL-2 production and Ca2+ mobilization after CD3 stimulation.

Perez VL, Rowe T, Justement JS, Butera ST, June CH, Folks TM.

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Division of Viral and Rickettsial Diseases, Centers for Disease Control, Atlanta, GA 30333.

Abstract

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.

PMID:: 1833465; [PubMed - indexed for MEDLINE]

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An HIV-1-infected T cell clone defective in IL-2 production and Ca2+ mobilization after CD3 stimulation.

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