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(Journal of Leukocyte Biology. 2001;69:361-372.)
© 2001 by Society for Leukocyte Biology

Retinoic acid up-regulates myeloid ICAM-3 expression and function in a cell-specific fashion—evidence for retinoid signaling pathways in the mast cell lineage

Department of Dermatology, Charité, Humboldt-Universität zu Berlin, Germany

Correspondence: Magda Babina, Department of Dermatology, Charité, Campus Virchow, Humboldt-Universität zu Berlin, Augustenburger Platz 1, D-13344 Berlin, Germany. E-mail: magda.babina{at}charite.de

Investigation of mast cell responsiveness toward retinoic acid (RA) revealed selective promotion of ICAM-3 expression in the human mast cell line HMC-1. This process was dose- and time-dependent and detectable by flow cytometry, Western blot analysis, ELISA, and Northern blot analysis. ICAM-3 modulation was found to be cell-type dependent, detectable also for HL-60 cells and monocytes but not U-937 and only weakly for KU812 cells. Terminally differentiated skin mast cells also failed to up-modulate their ICAM-3, suggesting the requirement for some degree of immaturity for the process. RA-mediated effects on ICAM-1 expression, studied in parallel, were clearly distinct from those on ICAM-3. Investigation of retinoid receptor expression, known to mediate intracellular RA signaling, revealed presence of RAR, RAR, RXRß, and RXR transcripts in all cell lines studied, and HMC-1 cells were the only line lacking RXR. RARß, not expressed at baseline, was induced by RA in a fashion obviously correlating with ICAM-3 up-regulation. Increased ICAM-3 expression was of functional significance, such that processes stimulated or co-stimulated via ICAM-3 (homotypic aggregation, IL-8 secretion) were clearly enhanced upon RA pretreatment, suggesting that RA may contribute via hitherto unrecognized pathways to immune function and host defense.

Key Words: vitamin A metabolites • adhesion molecules • homotypic aggregation • interleukin-8

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