Transforming growth factor β modulates C3 and factor B biosynthesis and complement receptor 3 expression in cultured human monocytes

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Abstract
Complement biosynthesis in monocytes is stimulated by different pathogens and modulated by a variety of cytokines, but little is known about the possible effect of transforming growth factor β (TGF-β) on this monocyte function. We therefore studied the effect of TGF-βl and TGF-β2 on constitutive, lipopolysaccharide (LPS)- and Candida albicans-induced monocyte biosynthesis of complement components C3 and factor B. Under all three conditions, both forms of TGF-β (20 ng/ml) induced a two- to fourfold increase in C3 concentration in monocyte supernatants harvested after 2 or 5 days of cell culture, an effect that was abrogated by cycloheximide. In contrast, constitutive and pathogen-induced production of factor B was suppressed by TGF-β. The effects of TGF-β on complement production were neutralized by a monoclonal anti-TGF-β antibody. Moreover, TGF-β suppressed the pathogen-induced release of granulocyte-macrophage colony-stimulating factor and down-regulated the expression of complement receptor 3 (CD11b/CD18), while the expression of CD11a/CD18, a related β 2 integrin, was unaffected. These novel effects of TGF-β emphasize the immunomodulatory significance of this cytokine. J. Leukoc. Biol. 57: 287–296; 1995.

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