The IL-17-producing CD4 + T cell and gamma delta T cells play critical roles in the pathogenesis of psoriasis (PS). PSORI-CM02 is a representative herbal formula for the treatment for PS in South China. It was confirmed to improve PS without obvious side effects in the clinic. Here we sought to clarify whether and how PSORI-CM02 regulates T cell differentiation and functions in IMQ-induced psoriasis-like BALB/c mouse model. Mice pre-treated 3 days with PSORI-CM02 significantly alleviated skin inflammation, as reduced in PASI score and classic psoriatic characteristics in pathological sections. CD3 and CD4 positive T cells were also fewer in the skin lesions of PSORI-CM02 groups, comparing to control group. PSORI-CM02 also decreased pro-inflammatory IFN gamma mRNA and IL-17A mRNA, while increased IL-4 mRNA in mouse skin lesions. In skin draining lymph nodes (DLN), PSORI-CM02 reduced the ratio of gamma delta T cells and inhibited their function of producing IL-17A. Nevertheless PSORI-CM02 had no effects on the ratio of total TCR beta + T cells and CD4 + T cells. But it regulated CD4 + T helper cells differentiation, and resulted in the decreasing percentage of IFN gamma producing Th1 cells and IL-17A producing Th17 cells, while increasing the ratio of IL-4 producing Th2 cells in DLN. Further data showed that PSORI-CM02 promote expression of Th2 specific transcript factor GATA3, but had no effects on T-bet and ROR gamma. Thus, we tentatively interpret that PSORI-CM02 impairs IMQ-induced psoriasis by promoting Th2 cell response targeting of GATA3.