Type I CD8+ cytotoxic T (Tc1) cells secrete IFN-γ and kill islet β-cells by either perforin or Fas-mediated mechanisms. IFN-γ secreting Th1 cells also play important roles in the destruction of β-cells as activators of cytotoxic CD8+ T cells. Tc17 cells producing IL-17, which has recently been identified, is remarkably noncytotoxic with little expression of granzyme B, perforin, and Fas ligand. A new T cell subset, T helper type 17 (Th17) cells, are increased in many models of autoimmunity and are often considered to be the principal driver of inflammation. And recently, Th22 cells producing IL-22 is considered to participating in the pathology of inflammation, tumors, and autoimmune diseases.
In order to find out the number of inflammatory T cells in blood of T1D patients, as well as the relative importance of each cell type, 5-color flow cytometry was used to identify and quantify Th1, Th17, Th22, Tc1, and Tc17 cells among circulating primary CD4+ or CD8+ T cells isolated from 42 individuals at different stages of T1D and 30 healthy controls. We also examined the serum IL-22 and IL-17 levels by ELISA.
Th17-Th22 and Tc1-Tc17 were significantly elevated in patients with T1D compared to control subjects, while there were no significant differences in Th1 cells. Th17, Th22 and Tc17 cells have the highest percentages in patients with early stages of T1D (<5 years), and retained or decreased slightly with progression of the disease. Th22 cells showed a positive correlation with Th17 cells in T1D patients. However, we did not find any correlation between IL-17 and IL- 22 in sera. This study indicates that Th22 may contribute to the pathogenesis of T1D. Blockade of Th22 cells might be of clinical profit in T1D patients.