Psoriasis vulgaris is a recurrent inflammatory skin disease. A variety of factors, such as trauma and infection, can destroy the skin barrier function, thereby breaking the balance of immune homeostasis and tolerance, causing abnormalities in function and/or number of various immune-related cells in local skin, resulting in psoriasis-like skin changes such as abnormal proliferation of keratinocytes and excessive inflammatory reactions in skin lesions. Various immune cells in skin lesions can sense changes in the surrounding environment (autocrine or paracrine) through surface molecules, and then express and secrete a variety of inflammation-related factors; if maintenance mechanisms for immune homeostasis and tolerance become invalid, the positive feedback network of inflammation mediated by inflammation-related factors will be formed locally, leading to the occurrence of psoriasis vulgaris. This review summarizes research progress in the role of immune-related cells in skin lesions in the immunopathological mechanism of psoriasis vulgaris, especially innate immune cells such as γδT cells.