Acne vulgaris is a skin disease that often occurs in adolescence and in young adulthood. The main pathogenic factors are hyperkeratinization, obstruction of sebaceous glands, stimulation of sebaceous gland secretion by androgens, and bacterial colonization of sebaceous units by Cutibacterium acnes, which promotes inflammation. Little is known about the role of skin immune cells in the development of acne lesions. The aim of the study was to try to understand the role of skin immune cells in the course of acne. Recent studies have shown that there are at least four major pathways by which Cutibacterium acnes interacts with the innate immune system to induce inflammation: through TLRs, activating inflammasomes, inducing the production of matrix metalloproteinases (MMPs), and stimulating antimicrobial peptide (AMP) activity. Cells of adaptive immune response, mainly Th1 and Th17 lymphocytes, also play an important role in the pathogenesis of acne. It is worth emphasizing that understanding the role of the skin's immune cells in the pathogenesis of acne may, in the future, contribute to the application of modern therapeutic strategies that would avoid addiction to antibiotics, which would alleviate the spectrum of resistance that is now evident and a current threat.
Keywords: AMP; MMP; Th1 and Th17 lymphocytes; acne vulgaris; treatment.