A diminished antigen presentation of blood monocytes to autologous T cells has been recently described in patients with rheumatoid arthritis (RA). In this study the defective presentation of common recall antigens by blood monocytes revealed it to be a monocyte dysfunction specific for RA which could not be found in other chronic inflammatory rheumatic or non-rheumatic diseases and which could be restored by recombinant human interferon gamma. In addition, RA monocytes in blood exhibited a strongly reduced expression of HLA-DR determinants on the cell surface. T cells from RA patients produced almost normal interleukin-2 (IL-2) levels and showed a normal IL-2 sensitivity after phytohemagglutinin (PHA) stimulation. Several reasons may be responsible for this altered monocyte function in RA. Among these an in vivo "preactivation" of monocytes associated with a reduced antigen-presenting capacity or an impaired regulation of monocyte/macrophage differentiation are discussed.