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 G1-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).
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Conference Article| October 26 2004
Vitamin A regulates proliferation and apoptosis of human T- and B-cells
H.K. Blomhoff 1
1Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, P.O. Box 1112, Blindern, N-0317 Oslo, Norway
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Biochem Soc Trans (2004) 32 (6): 982–984.
June 18 2004
H.K. Blomhoff; Vitamin A regulates proliferation and apoptosis of human T- and B-cells. Biochem Soc Trans 1 November 2004; 32 (6): 982–984. doi: https://doi.org/10.1042/BST0320982
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