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ORIGINAL RESEARCH ARTICLE

Retinoic Acid Regulates CD1d Gene Expression at the Transcriptional Level in Human and Rodent Monocytic Cells

Qiuyan Chen^* and A. Catharine Ross^,1

^* Department of Nutritional Sciences and Huck Institute for Life Sciences, Pennsylvania State University, University Park, Pennsylvania 16802

To whom requests for reprints should be addressed at ¹ Department of Nutritional Sciences, Pennsylvania State University, 126-S Henderson Building, University Park PA 16802. E-mail: acr6{at}psu.edu

CD1d belongs to a group of nonclassical antigen-presenting molecules that present glycolipid antigens and thereby activate natural killer T (NKT) cells, a subset of bifunctional T cells. Little is known so far regarding the expression and physiologic regulation of CD1d. Here we show that all-trans-retinoic acid (RA), the active metabolite of vitamin A, rapidly (1 hr after treatment) increases CD1d mRNA in human and rodent monocytic cells at a physiologic dose (10 nM). The induction is RA specific and RA receptor (RAR) dependent—RA and an RAR agonist, Am580, both had a pronounced positive effect, whereas the addition of RAR antagonist partially blocked the increase in CD1d mRNA induced by RA and Am580. The induction was also completely blocked by the presence of actinomycin D. A putative RA-response element was identified in the distal 5' flanking region of the CD1d gene, which binds nuclear retinoid receptors and was responsive to RA in both gel mobility shift assay and transient transfection assay in THP-1 cells. These results further confirmed the transcriptional regulation of RA in CD1d gene expression. Moreover, RA significantly increased -galactosylceramide-induced spleen cell proliferation. These studies together provide evidence for a previously unknown mechanism of CD1d gene expression regulation by RA and suggest that RA is a significant modulator of NKT cell activation.

Key Words: gene expression • promoter • -galactosylceramide • retinoic acid response element

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