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Chronic inflammatory skin diseases are multifactorial diseases that combine genetic predisposition, environmental triggers, and metabolic disturbances associated with abnormal immune responses. From an immunological perspective, the better understanding of their physiopathology has demonstrated a large complex network of immune cell subsets and related cytokines that interact with both epidermal and dermal cells. For example, in type-1-associated diseases such as alopecia areata, vitiligo, and localized scleroderma, recent evidence suggests the presence of a type-2 inflammation that is well known in atopic dermatitis. Whether this type-2 immune response has a protective or detrimental impact on the development and chronicity of these diseases remains to be fully elucidated, highlighting the need to better understand its involvement for the management of patients. This mini-review explores recent insights regarding the potential role of type-2-related immunity in alopecia areata, vitiligo, and localized scleroderma.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11167106 | PMC |
http://dx.doi.org/10.3389/fimmu.2024.1405215 | DOI Listing |
Clin Cosmet Investig Dermatol
September 2025
Department of Dermatology, State Key Laboratory of Complex Severe and Rare Diseases, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, Beijing, 100730, People's Rep
Purpose: Alopecia areata (AA) is a common, immune-mediated, non-scarring form of hair loss. Janus kinase inhibitors provide considerable insight into the treatment of severe AA. However, the efficacy and safety of upadacitinib treatment of adolescents and pediatric patients with severe AA is unclear, especially in those without concomitant atopic diseases.
View Article and Find Full Text PDFFront Immunol
September 2025
Department of Dermatology, The National Center for the Integration of Traditional Chinese and Western Medicine, China-Japan Friendship Hospital, Beijing, China.
Background: Bullous Pemphigoid (BP) is caused by a predominantly Th2-mediated attack on the basement membrane by the production of anti-BP180 and anti-BP230 antibodies. Malignant tumors can exacerbate immune disorders through a variety of potential pathways, including pro-inflammatory responses in the tumor microenvironment, cross-immune responses induced by tumor-associated antigens, and the lifting of immunosuppressive states and activation of underlying autoimmune responses after surgery. Alopecia Areata (AA) is an autoimmune disease caused by T-lymphocyte-mediated destruction of the immune privilege of the hair follicle, specifically involving the immune axes of Th1, Th2 and Th17.
View Article and Find Full Text PDFTelemed Rep
August 2025
Medical Center Department of Dermatology, University of Pittsburgh, Wexford, Pennsylvania, USA.
Background: Non-scarring alopecia, including androgenetic alopecia (AGA), alopecia areata (AA), telogen effluvium (TE), and traction alopecia (TA), significantly impacts psychosocial well-being. Access to specialized dermatologic care for these conditions is often limited, particularly in underserved populations. Asynchronous teledermatology has emerged as a potential solution to extend care to these groups.
View Article and Find Full Text PDFJ Dermatolog Treat
December 2025
Department of Dermatology, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.
Objectives: Baricitinib showed efficacy for alopecia areata (AA) in clinical trials, with real-world data supporting its short-term effectiveness. However, long-term data are limited. We assessed the effectiveness and safety of baricitinib in AA patients over one year and explored predictive factors.
View Article and Find Full Text PDFJ Drugs Dermatol
September 2025
Background: Alopecia universalis (AU) is the most severe form of alopecia areata (AA), characterized by complete scalp and body hair loss. While post-COVID-19 hair loss is often attributed to telogen effluvium (TE), emerging evidence suggests that COVID-19 may also trigger AU through immune dysregulation, particularly via interferon-gamma (IFN-γ)-mediated inflammation. The chronic and relapsing nature of AU raises challenges in long-term disease management, particularly regarding treatment duration and relapse prevention.
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