Figure 3.

Sequential involvement of immune cells in different types of acne lesions and the critical events that drive the initiation and progression of acne. The dysbiosis of microorganisms, sebum, neuroactivity, or environmental virulence factors triggers the initiation of an immune response. At this stage, immune cells have already infiltrated the skin without any visible clinical lesions (non-lesional skin). This early-stage immune activity induces the hypercornification of the hair infundibulum and overstimulates sebocyte function, resulting in the formation of microcomedones and later comedones. C. acnes multiplies during the development of comedones. Continued stress from C. acnes and the enlargement of comedones on the hair follicles result in the rupture of the follicle wall. The contents of the comedones, including microorganisms, sebum and keratin squamae are released into the dermis, leading to the formation of papules or pustules. Ultimately, if the inflammation intensifies without control, papules or pustules may develop into more severe lesions, such as nodules and cysts. The sequential involvement of immune cells currently observed in different types of acne lesions is summarized in the corresponding text box. Further studies are needed to obtain more information, including the cell numbers, tissue localization, differentiation and migration trajectory, as well as the biological functions of specific immune cells involved in different acne lesions. Moreover, it is crucial to elucidate the molecular mechanisms that underlie these characteristics to facilitate the development of targeted treatment and prevention strategies for acne.