1α,25-dihydroxyvitamin D3 induces maturation of the human monocyte cell line U937, and, in association with a factor from human T lymphocytes, augments production of the monokine, mononuclear cell factor

E. P. Amento, A. K. Bhalla, J. T. Kurnick, R. L. Kradin, T. L. Clemens, S. A. Holick, M. F. Holick, S. M. Krane

Research output: Contribution to journalArticlepeer-review

Abstract

The monocyte factor, interleukin 1, or other factors homologous with interleukin 1, modulates functions of a variety of cells, including T and B lymphocytes, synovial cells, and chondrocytes. We have reported that a human monocyte cell line, U937, produces interleukin 1 when incubated with a soluble factor from lectin-stimulated T lymphocytes. We have also shown that U937 cells have a specific cytosolic receptor for 1α,25-dihydroxyvitamin D3 (1α,25[OH]2D3). We now report that 1α,25[OH]2D3 (10-11-10-10 M) induces maturational changes in the U937 cells similar to those produced by conditioned medium from lectin-stimulated T lymphocytes (increase in Fc receptors and OKM1 binding and decrease in proliferation), but does not induce monokine production as measured by mononuclear cell factor activity. 1α,25[OH]2D3 is 200-300-fold more effective than 25-hydroxyvitamin D3, which is consistent with the known biological potency of these vitamin D3 metabolites. 1α,25[OH]2D3 and the lymphokine together markedly augment maturational effects and, in addition, augment monokine production. The specificity of the interaction is further demonstrated by the lack of augmentation of monokine production with 1β,25[OH]2D3 in the presence of lymphokine. These interactions of a classical hormone and the hormonelike product(s) of the immune system with U937 cells serve as a model for human monocyte/macrophage differentiation and suggest a role for these interactions in some aspects of inflammation.

Original languageEnglish (US)
Pages (from-to)731-739
Number of pages9
JournalJournal of Clinical Investigation
Volume73
Issue number3
DOIs
StatePublished - 1984
Externally publishedYes

ASJC Scopus subject areas

  • Medicine(all)

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