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The cell surface molecule CD6 is a modulator of T cell receptor (TCR) signaling. Recently, it has been reported that CD6 is downregulated on CD4+ T cells following T cell activation. This mechanism could limit the efficacy of anti-CD6 therapeutical antibodies. We analyzed CD6 expression on activated and non-activated Th1 cells and Th17 cells by flow cytometry. Our experiments confirmed a significant downregulation of CD6 on IFNγ- and IL17-negative CD4+ T cells from healthy individuals and from patients with rheumatoid arthritis following T cell activation with anti-CD3 and anti-CD28 antibodies. In contrast, CD6 expression remained stable on activated Th17 cells and Th1 cells. Th1 and Th17 cells are resistant towards T cell activation-induced downregulation of CD6. These findings are relevant for the future development of CD6 targeting therapies and show that CD6 expression is differentially regulated in CD4+ T cell subsets. • CD6 is downregulated by T cell activation in IFNg- and IL17-negative CD4+ T cells, but not in Th1 and Th17 cells • Resistance towards activation-induced CD6 downregulation is also found in Th1 and Th17 cells from RA patients. • These findings indicate that CD6 is a suitable antigen to target Th1 and Th17 cells in RA. [ABSTRACT FROM AUTHOR]