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The Journal of Immunology, Vol 155, Issue 1 58-65, Copyright © 1995 by American Association of Immunologists
ARTICLES |
C Fahlman, SE Jacobsen, EB Smeland, J Lomo, CE Naess, S Funderud and HK Blomhoff
Department of Immunology, Norwegian Radium Hospital, Montebello, Oslo.
In the present paper we demonstrate that physiologic levels (10 nM) of both all-trans- and 9-cis-retinoic acid (RA) are potent inhibitors of the growth of human as well as murine B cell precursors in vitro. Ten nanomolar concentrations of all-trans- and 9-cis-RA reduced the DNA synthesis ([3H]thymidine uptake) of human B cell precursors (CD19+ IgM- ) stimulated with O-tetradecanoylphorbol-13-acetate and ionomycin by approximately 55% and 70%, respectively. Human B cell precursors stimulated with low m.w. B cell growth factor were also inhibited by RA. Ten nanomolar concentrations of either isoform of RA reduced DNA synthesis by approximately 50%. No effect of RA on differentiation to sIgM positive cells was noted. The potent growth-inhibiting effect of RA on human B cell precursors was confirmed in the murine cell system. B lymphopoiesis from murine hematopoietic precursors (Lin-B220(+)- containing cells) was induced by stimulation with IL-7. Concentrations of all-trans- and 9-cis-RA as low as 10 pM reduced the colony-forming ability of the IL-7-stimulated Lin-B220(+)-containing cells. Ten nanomolar concentrations of either isoform reduced colony formation by approximately 60%. RA was not toxic to the cells, as the inhibition of colony formation after 24 h was reversible at concentrations as high as 1 microM. The growth-inhibiting effect of RA was directly mediated, as revealed by single cell analysis of the Lin-B220(+)-containing cells. Thus, vitamin A appears to have an important role in regulation of B lymphopoiesis.
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