Abstract
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.
Highlights
IntroductionThe main pathogenic factors of acne include hyperkeratinisation, the secretion from the sebaceous glands stimulated by androgens, dysbiosis of the skin microbiome, and Cutibacterium acnes (C. acnes); and the overcolonisation of pilosebaceous units, which might provide favourable conditions for perifolliculitis
Manfredini M. et al [5] assessed the evolution of acne lesions from clinically unchanged skin in mild to moderate acne patients using in vivo reflection confocal microscopy (RCM) and dynamic optical coherence tomography (D-OCT)
Histological studies showed that CD4+ T cells were the most numerous cells of the white blood cell system in early-stage inflammatory infiltrations (6–72 h) in acne lesions, which suggests that they might take part in immune response triggered by the colonization of the sebaceous gland by C. acnes [42]
Summary
The main pathogenic factors of acne include hyperkeratinisation, the secretion from the sebaceous glands stimulated by androgens, dysbiosis of the skin microbiome, and Cutibacterium acnes (C. acnes); and the overcolonisation of pilosebaceous units, which might provide favourable conditions for perifolliculitis. LRIG cells can differentiate toward epithelial or sebaceous type and should, be prime targets for comedogenic factors. This population can, be a source of blackhead lesions. Manfredini M. et al [5] assessed the evolution of acne lesions from clinically unchanged skin in mild to moderate acne patients using in vivo reflection confocal microscopy (RCM) and dynamic optical coherence tomography (D-OCT). The objective of the paper is to explore the role of the cells of the skin immune system in the course of acne. Therapeutic success may be achieved thanks to the understanding and processes accounting for immunology processes taking place in skin and hair follicles
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