Abstract: Psoriasis is chronic autoimmune inflammatory skin disease and its pathogenesis has not been fully understood. Absent in melanoma 2 (AIM2) is a sensor involved in innate immune response, can recognize double stranded deoxyribonucleic acid (dsDNA) and further assemble them into AIM2 inflammosome. AIM2 inflammasome is a protein complex, while inappropriate recognition of cytoplasmic self-DNA by AIM2 contributes to the development of psoriasis, atopic dermatitis, arthritis and other autoimmune as well as inflammatory diseases. Therefore, inhibition of AIM2 inflammasome activation is expected to be a new therapeutic target for psoriasis. This article reviewed the mechanism of AIM2 in psoriasis and the evidence of AIM2 inflammasome involving in the pathogenesis of experimental psoriasis model.