MODULATION OF IGA, IGE, AND IGG FC RECEPTOR EXPRESSION ON HUMAN MONONUCLEAR PHAGOCYTES BY 1-ALPHA,25-DIHYDROXYVITAMIN D-3 AND CYTOKINES

Citation
G. Boltznitulescu et al., MODULATION OF IGA, IGE, AND IGG FC RECEPTOR EXPRESSION ON HUMAN MONONUCLEAR PHAGOCYTES BY 1-ALPHA,25-DIHYDROXYVITAMIN D-3 AND CYTOKINES, Journal of leukocyte biology, 58(2), 1995, pp. 256-262
Citations number
54
Categorie Soggetti
Immunology,Hematology
ISSN journal
07415400
Volume
58
Issue
2
Year of publication
1995
Pages
256 - 262
Database
ISI
SICI code
0741-5400(1995)58:2<256:MOIIAI>2.0.ZU;2-L
Abstract
The effects of 1 alpha,25-dihydroxyvitamin D-3/calcitriol on the expre ssion of Fc receptors (FcR) for IgA (Fc alpha R), IgE (Fc epsilon RII) , and IgG (Fc gamma R) on human peripheral blood monocytes and the cel l lines U937, THP-1, and Mono Mac-6, in combination with various cytok ines, was examined by flow cytometry, On both monocyte derived macroph ages and the myelomonocytic cell lines, Fc alpha R/CD89 expression was induced by calcitriol alone and additively in combination with tumor necrosis factor-alpha (TNF-alpha), interferon-gamma (IFN-gamma), and g ranulocyte-macrophage colony-stimulating factor, Constitutive and inte rleukin-4 (IL-4)-driven Fc epsilon RII/CD23 expression was markedly di minished on calcitriol-treated U937 cells and monocytes, Fc epsilon RI I was also triggered by IFN-gamma, TNF-alpha, and IL-6 on all the cell lines, an effect blocked by calcitriol, On monocytes, the basal level and IFN-gamma-induced Fc gamma RI/CD64 expression was down-regulated by calcitriol and IL-4, The expression of Fc gamma RII/CD32 on monocyt es was strongly suppressed by calcitriol. Transforming growth factor-P induced Fc gamma RII/CD16 on monocytes, an effect opposed by calcitri ol, The ability of calcitriol-treated monocytes to phagocytose IgG-sen sitized ox erythrocytes was diminished, Our results demonstrate that c alcitriol, alone or in combination with cytokines, modulates Fc alpha R, Fc epsilon RII, Fc gamma RI, and Fc gamma RII expression on human m ononuclear phagocytes, as well as Fc gamma R-mediated phagocytosis.