HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEIN GP120 PRODUCES IMMUNE DEFECTS IN CD4+ LYMPHOCYTES-T BY INHIBITING INTERLEUKIN-2 MESSENGER-RNA
HUMAN-IMMUNODEFICIENCY-VIRUS TYPE-1 ENVELOPE GLYCOPROTEIN GP120 PRODUCES IMMUNE DEFECTS IN CD4+ LYMPHOCYTES-T BY INHIBITING INTERLEUKIN-2 MESSENGER-RNA
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DOI:
10.1073/pnas.87.6.2379
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发表时间:
1990-03-01
影响因子:
11.1
通讯作者:
PAHWA, S
中科院分区:
文献类型:
--
作者:
OYAIZU, N;CHIRMULE, N;PAHWA, S
Envelope glycoprotein gp120 of human immunodeficiency virus type 1 (HIV-1) is known to inhibit T-cell function, but little is known about the mechanisms of this immunosuppression. Pretreatment of a CD4+ tetanus toxoid-specific T-cell clone with soluble gp120 was found to exert a dose-dependent inhibition of soluble antigen-driven or anti-CD3 monoclonal antibody-driven proliferative response, interleukin 2 (IL-2) production, and surface IL-2 receptor (IL-2R) alpha-chain expression, all of which were reversed by the addition of exogenous IL-2. mRNA for the gene encoding IL-2 was suppressed by treatment with gp120, but IL-2R gene transcription was not inhibited. Bypass activation of the T-cell clone with phorbol 12-myristate 13-acetate plus ionomycin was unaffected by gp120 pretreatment. Thus, gp120-CD4 interaction interferes with an essential role of the CD4 molecule in signal transduction through the CD3-antigen receptor (Ti) complex. Such a mechanism of gp120-induced immunosuppression, if operative in vivo, could contribute to the depressed specific immune responses associated with HIV infection.