To elucidate the resistance of CD4+ T cells to this direct inhibition in RA, we investigated the production of IFN-γ after CD3 and CD28 costimulation in the presence of IL-10, the induction of STAT1 and STAT3 phosphorylation by IL-10, and the expression of SOCS1 and SOCS3 mRNA in peripheral blood (PB) CD4+ T cells from RA patients. Here, STAT1 is linked to rheumatoid arthritis.