Interleukin (IL)-22 regulates the pathogenesis of autoimmune diseases. The role of IL-22(+) T-cells in the pathogenesis of rheumatoid arthritis (RA) is unclear. This study aimed at examining the levels of plasma IL-22 and the frequency of IL-22(+) CD4(+) T-cells in patients with RA.
A total of 30 RA patients and 18 gender- and age-matched healthy controls were recruited. Their peripheral blood mononuclear cells were isolated and stimulated with phorbol 12-myristate 13-acetate (PMA) and ionomycin for 6 h. The frequency of IL-22(+) , interferon (IFN)-γ(+) and IL-17A(+) CD4(+) T-cells was characterized by flow cytometry. The levels of plasma IFN-γ, IL-17A and IL-22, serum C-reactive protein (CRP), rheumatoid factor (RF), anticyclic citrullinated peptide antibody (CCP) and erythrocyte sedimentation rate (ESR) were measured.
The frequency of IFNγ(-) IL-17A(-)IL-22(+), IFNγ(-)IL-17A(+)IL-22(+), and IFNγ(+) IL-17A(-)IL-22(+) T-cells in CD4(+) T-cells and the levels of plasma IFNγ, IL-17 and IL-22 in RA patients were significant higher than those in healthy controls. The percentages of IL-17A(+)IL-22(+)CD4(+) T-cells were correlated positively with the frequency of Th22 or Th17 cells in the RA patients. The percentages of IL-22(+)CD4(+) T-cells were correlated positively with the values of disease activity score (DAS28) in the RA patients. The percentages of Th22 cells were correlated positively with the levels of plasma IL-22 in the RA patients.
Our data suggest that IL-22(+)CD4(+) T-cells may contribute to the pathogenesis of RA and that therapeutic targeting of IL-22 may be valuable for the intervention of RA.