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• W2068841623 abstract "Signalling through CD4 by human immunodeficiency virus (HIV)-1 envelope glycoprotein (gpl20) and/or anti-CD4 antibodies can promote T-cell activation and anergy. Interleukin (IL)-16 is a competence growth factor for CD4+ T cells that can induce a G0 to G1 cell cycle transition but cannot induce cell division. The receptor of this cytokine is thought to be the CD4 molecule, although the binding epitope of IL-16 differs from that of HIV. We have demonstrated that both HIV-1/gp120 and IL-16 induced CD4+ T-cell dysfunction, as indicated by suppression of mitogen-induced IL-2 production. Two anti-CD4 antibodies with different binding sites on CD4 also showed an inhibitory effect on IL-2 production. These results indicate that promotion of CD4+ T-cell anergy via the CD4 molecule does not depend on the binding sites of the CD4 ligands." @default.
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• W2068841623 date "1999-02-01" @default.
• W2068841623 modified "2023-10-09" @default.
• W2068841623 title "Inhibitory effect of interleukin‐16 on interleukin‐2 production by CD4⁺T cells" @default.
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• W2068841623 doi "https://doi.org/10.1046/j.1365-2567.1999.00693.x" @default.
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