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

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...

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Published inThe Journal of immunology (1950) Vol. 147; no. 9; pp. 3145 - 3148
Main Authors Perez, VL, Rowe, T, Justement, JS, Butera, ST, June, CH, Folks, TM
Format Journal Article
LanguageEnglish
Published Bethesda, MD Am Assoc Immnol 01.11.1991
American Association of Immunologists
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Summary: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.
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ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.147.9.3145