Skin immunity and its dysregulation in atopic dermatitis, hidradenitis suppurativa and vitiligo
- 5 January 2020
- journal article
- review article
- Published by Taylor & Francis Ltd in Cell Cycle
- Vol. 19 (3), 257-267
- https://doi.org/10.1080/15384101.2019.1707455
Abstract
While the epidermis is the frontline defense against infections and indeed, it is a peripheral lymphoid organ, the same immunological mechanisms may initiate and sustain pathological conditions. Indeed, a deregulated action against exogenous pathogens could activate a T cell response in atopic dermatitis, hidradenitis suppurativa and vitiligo. Atopic dermatitis (AD) is a chronic inflammatory skin condition with a complex pathophysiology. Although T helper 2 immunity dysregulation is thought to be the main cause of AD etiopathogenesis, the triggering mechanism is not well understood, and the treatment is often difficult. As the AD, hidradenitis suppurativa (HS) is a chronic inflammatory skin disease with a dramatic impact on the quality of life of the affected patients. The exact pathophysiology of HS is still unclear, but many evidences report a follicular obstruction and subsequent inflammation with TNF-α, interleukin (IL)-1β, IL-10, and IL-17 involvement. Vitiligo is an autoimmune epidermal disorder which consists of melanocytes destruction and skin depigmentation. Melanocytes destruction is mainly due to their increased oxidative-stress sensitivity with a consequent activation of innate first and adaptative immunity (CD8+ T cells) later. The understanding of the triggering mechanisms of AD, HS and Vitiligo is pivotal to outline novel therapies aimed at regaining the physiological immune homeostasis of healthy skin. The aim of this review is to provide new insight on the pathogenesis of these skin diseases and to highlight on the new therapeutic approaches adopted in the treatment of AD, HS and Vitiligo.Keywords
Funding Information
- Associazione Italiana per la Ricerca contro il Cancro (GM IG#20473)
- Ministry of Health Italy–China cooperation
- Regione Lazio through Lazio Innova Progetto Gruppo di Ricerca
This publication has 130 references indexed in Scilit:
- p63–microRNA feedback in keratinocyte senescenceProceedings of the National Academy of Sciences of the United States of America, 2012
- ΔNp63 is an ectodermal gatekeeper of epidermal morphogenesisCell Death & Differentiation, 2010
- Generation of pathogenic TH17 cells in the absence of TGF-β signallingNature, 2010
- Skin immune sentinels in health and diseaseNature Reviews Immunology, 2009
- IL-22–producing “T22” T cells account for upregulated IL-22 in atopic dermatitis despite reduced IL-17–producing TH17 T cellsJournal of Allergy and Clinical Immunology, 2009
- TAp73 regulates the spindle assembly checkpoint by modulating BubR1 activityProceedings of the National Academy of Sciences of the United States of America, 2009
- T-Helper 17 Cells in Psoriatic Plaques and Additional Genetic Links between IL-23 and PsoriasisJournal of Investigative Dermatology, 2008
- Loricrin and involucrin expression is down-regulated by Th2 cytokines through STAT-6Clinical Immunology, 2008
- The cornified envelope: a model of cell death in the skinNature Reviews Molecular Cell Biology, 2005
- Cytokines and autoimmunityNature Reviews Immunology, 2002