Inhibitory effect of interleukin-16 on interleukin-2 production by CD4+ T cells.
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.
Ogasawara
H
H
Department of Internal Medicine and Rheumatology, Juntendo University School of Medicine, Hongo, Tokyo, Japan.
Takeda-Hirokawa
N
N
Sekigawa
I
I
Hashimoto
H
H
Kaneko
Y
Y
Hirose
S
S
D000906:Antibodies / Q000494:pharmacology; D001665:Binding Sites; D015704:CD4 Antigens / Q000276:immunology; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D016827:CD8 Antigens / Q000276:immunology; D017635:Clonal Anergy / Q000276:immunology; D003208:Concanavalin A / Q000494:pharmacology; D004797:Enzyme-Linked Immunosorbent Assay; D015699:HIV Envelope Protein gp120 / Q000494:pharmacology; D006801:Humans; D019410:Interleukin-16 / Q000494:pharmacology*; D007376:Interleukin-2 / Q000378:metabolism*
D000906:Antibodies; D015704:CD4 Antigens; D016827:CD8 Antigens; D015699:HIV Envelope Protein gp120; D019410:Interleukin-16; D007376:Interleukin-2; D003208:Concanavalin A