It is unclear how to promote pathogenic Th17-responses in psoriasis. In this report, we proposed a possibility of involvement of Th17 subsets in the pathogenesis. We found that CD31-CCR6+ population in naïve type CD4 T cells excluded MAIT cells could develop into IL-17 producing cells after TCR-stimuli with IL-1b and IL-23. Intriguingly, those activated T cells included heterogeneous RORC2+ cells that express not only IL-17 but also IFN-g, IL-10, or Foxp3. Such naive type CCR6+ CD4 T cells were significantly increased in psoriatic patients in comparison with healthy volunteers, and the increase correlated to severity of the disease (r=0.518, n=49, P<0.05). Thereafter, we analyzed heterogeneous populations derived from CD31-CCR6+ naïve type CD4 T cells due to marking putative human Th17-cell surface markers (IL-23R, MCAM and CD161). Highly purified four populations (IL-23R+MCAM+CD161+ cells, IL-23R-MCAM+CD161+ cells, IL-23R- MCAM+CD161- cells and IL-23R-MCAM-CD161+ cells were subjected to SAGE (serial analysis of gene expression). Intriguingly, IL-23R-MCAM+CD161- cells had unique characteristics such as no expression of PD-L1 that controls excessive immune reaction. Furthermore, CCR6+MCAM+CD161- population in effector memory CD4 T cells were predominately increased in psoriatic patients. These data suggest that the increased certain Th17 subsets derived from naïve type CCR6+ CD4 T cells could promote pathogenesis in psoriasis.