alexa IL-12 inhibits apoptosis induced in a human Th1 clone by gp120 CD4 cross-linking and CD3 TCR activation or by IL-2 deprivation.
Infectious Diseases

Infectious Diseases

Journal of AIDS & Clinical Research

Author(s): Radrizzani M, Accornero P, Amidei A, Aiello A, Delia D,

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Abstract The aim of our work was to study apoptosis as a possible mechanism of CD4+ lymphocyte depletion in AIDS patients and to test whether IL-12 could limit this phenomenon. As an in vitro model, we used a human IL-2-dependent Th1 clone from an uninfected individual. We found that CD4 cross-linking, obtained either by mouse anti-CD4 mAb plus goat anti-mouse or by recombinant gp120 plus anti-gp120 mAb, followed by activation with immobilized anti-CD3 or anti-TCR mAb, induced apoptosis at early times (15-25\% apoptotic cells at 4 hr), whereas IL-2 deprivation required longer times (20-40 hr) to induce apoptosis. Both CD4 cross-linking and IL-2 deprivation-induced apoptosis appeared to be PTK-dependent and were inhibited by either IL-2 or IL-12. Our data suggest that in vivo CD4/gp120 interactions could directly prime the apoptosis of Th1 lymphocytes and that IL-2 and IL-12 could be used to prevent this phenomenon. This article was published in Cell Immunol and referenced in Journal of AIDS & Clinical Research

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