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

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.