Atrophic scar formation in patients with acne involves long‐acting immune responses with plasma cells and alteration of sebaceous glands

BACKGROUND: Possible outcomes of acne lesions are atrophic scars which may cause serious psychological distress. Current treatments of post-acne scarring often require invasive procedures. Pathophysiological studies on acne scarring investigated only the first week of papule life. OBJECTIVES: Study the pathophysiology of atrophic scar formation to identify molecular and cellular pathways that can lead to new therapies for the prevention of acne scarring. METHODS: Large-scale gene expression profiling and immunohistochemistry analysis were performed on uninvolved skin and papules in both, scar-prone (SP) and non-scar-prone (NSP) acne patients, at different time points. RESULTS: Gene expression and immunohistochemistry analyses showed a very similar immune response in 48 hours-old papules in SP and NSP populations, characterized by elevated numbers of T cells, neutrophils and macrophages. However, only in SP patients the immune response persisted in 3 week-old papules, and was characterized by an important infiltrate of B cells. Transient down-modulation of sebaceous gland markers related to lipid metabolism was observed in 48 hours-old papules in NSP patients, followed by normalization after 3 weeks. In contrast, in SP patients a drastic reduction of these markers persisted in 3 week-old papules, suggesting an irreversible destruction of sebaceous gland structures after inflammatory remodelling in SP acne patients. CONCLUSIONS: Long lived acne papules are characterized by a B cell infiltrate. A relationship exists between the duration and severity of inflammation and the alteration of sebaceous gland structures, leading to atrophic scar formation in acne. This article is protected by copyright. All rights reserved.