Vitamin A regulates proliferation and apoptosis of human T- and B-cells.
Vitamin A is known to protect against infections, but it is not established how vitamin A metabolites stimulate the immune system. We have investigated the effects of physiological levels of retinoic acid on the function of normal human T- and B-cells. Surprisingly, we found that the proliferation of B-cells was inhibited by retinoids, and that this was due to rapid inhibition of the cell cycle machinery regulating G(1)-to-S transition. In contrast, the proliferation of T-cells was enhanced by physiological levels of retinoic acid, and the effect was due to induction of IL-2 (interleukin 2). The 'non-death-receptor'-mediated apoptosis of normal T-cells induced by prolonged (but single) stimulation of the cells was also prevented by retinoid acid, and also this effect was mediated via enhanced production of IL-2. The induction of IL-2 was at the transcriptional level, and all the effects of vitamin A on both B-and T-cells were mediated via the nuclear retinoic acid receptors (RARs), and not retinoid X receptors (RXRs).
Blomhoff
H K
HK
Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, P.O. Box 1112, Blindern, N-0317 Oslo, Norway. h.k.blomhoff@basalmed.uio.no
D017209:Apoptosis / Q000187:drug effects*; D001402:B-Lymphocytes / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D002455:Cell Division / Q000187:drug effects*; D006801:Humans; D007376:Interleukin-2 / Q000096:biosynthesis; D008213:Lymphocyte Activation / Q000187:drug effects; D013601:T-Lymphocytes / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D014801:Vitamin A / Q000494:pharmacology*
D007376:Interleukin-2; D014801:Vitamin A