Cloned human interferon-gamma, but not interferon-beta or -alpha, induces expression of HLA-DR determinants by fetal monocytes and myeloid leukemic cell lines.

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Abstract
The antigen presenting function of macrophages and other accessory cells requires the cell surface expression of class II major histocompatibility antigens, e.g., HLA-DR. It has been shown that gamma-interferon (IFN-gamma), a T cell product, can regulate macrophage HLA-DR expression. The effect of absolutely pure or cloned IFN-gamma upon fetal monocytes that do not strongly express DR has not been studied. We have utilized cloned IFN-gamma, IFN-beta, and IFN-alpha preparations to examine the differential effects of these molecules upon the expression of HLA class I (HLA-A,B) and class II determinants by fetal monocytes as well as by myeloid leukemic cell lines. We report that cloned human IFN-gamma induces the expression of HLA-DR and -A,B antigens on cells that normally express low quantities of these molecules, including human fetal monocytes and two (ML-1 and HL-60) but not a third (U-937) myeloid leukemic cell lines. These findings suggest that the acquisition of class II HLA molecules upon fetal tissues and perhaps antigen presenting function is dependent upon IFN-gamma. In contrast, IFN-beta and -alpha induced the expression of HLA-A,B but not HLA-DR antigens by these cells. Thus, these data indicate that the expression of HLA-DR molecules that is vital for monocyte/macrophage and T cell interaction is stimulated by the lymphokine IFN-gamma, and that the effects of IFN-gamma are distinctive from IFN-alpha or -beta.