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Biochemical Society Transactions (2004) 32, (982–984) (Printed in Great Britain)

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Vitamin A regulates proliferation and apoptosis of human T- and B-cells

H.K. Blomhoff¹

Department of Biochemistry, Institute of Basic Medical Sciences, University of Oslo, P.O. Box 1112, Blindern, N-0317 Oslo, Norway

Key words: apoptosis, cell cycle, human T- and B-cells, interleukin-2, lymphocytes, retinoic acid, vitamin A.

Abbreviations used: ACAD, activated T-cell autonomous death; CDK, cyclin-dependent kinase; CKI, CDK inhibitor; IL(-2), interleukin(-2); PHA, phytohaemagglutinin; pRB, retinoblastoma protein; RA, all-trans-retinoic acid; RAR, retinoic acid receptor; RXR, retinoid X receptor.

¹email h.k.blomhoff@basalmed.uio.no

Abstract

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).

Received 18 June 2004

© 2004 Biochemical Society