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Regulation of human monocyte HLA-DR and CD4 antigen expression, and antigen
presentation by 1,25-dihydroxyvitamin D3
WF Rigby, M Waugh and RF Graziano
Department of Microbiology, Dartmouth-Hitchcock Medical Center, Hanover,
NH.
1,25-Dihydroxyvitamin D3 (1,25(OH)2-D) has been shown to be a
macrophage-derived cytokine, capable of regulating myeloid differentiation
and T-cell activation in vitro. Therefore, we examined the effects of
1,25(OH)2-D on the monocyte phenotype and function of human peripheral
blood monocytes as an index of its biologic role at an inflammatory site.
1,25(OH)2-D treatment consistently and specifically reduced HLA-DR and CD4
expression by monocytes, while CD14 and class I HLA antigen expression were
unaffected. Expression of Fc gamma R I-III on monocytes was variably
modulated by 1,25(OH)2-D treatment, but no differences in
antibody-dependent cell cytotoxicity (ADCC) were observed, measured using
either ADCC or anti-Fc gamma R-antibody expressing hybridomas. In contrast,
the ability of monocytes to induce antigen-dependent T-cell proliferation
was markedly reduced by 1,25(OH)2-D pretreatment for as little as 6 hours.
Addition of interleukin-1 (IL-1), IL-6, or indomethacin did not restore
antigen- dependent T-cell proliferation, suggesting that this observation
was not secondary to changes in IL-1, IL-6, or PGE2 production induced by
1,25(OH)2-D. These data suggest that 1,25(OH)2-D treatment specifically
modulates human monocyte phenotype and function, altering HLA-DR antigen
expression and antigen presentation, while leaving lytic function intact.
These findings may be relevant to the immunobiologic role of 1,25(OH)2-D.
Volume 76,
Issue 1,
pp. 189-197,
07/01/1990
Copyright © 1990 by The American Society of Hematology
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