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Dissecting susceptibility from exogenous triggers: the model of alopecia areata and associated inflammatory skin diseases.
J Eur Acad Dermatol Venereol. 2015 Dec; 29(12):2429-35.JE

Abstract

BACKGROUND

Alopecia areata (AA) is a T-cell-driven autoimmune disease of the hair follicle and frequently reported to be associated with inflammatory skin diseases (ISD) such as atopic eczema (AE) or psoriasis. Interestingly, AA on the one hand and both AE and psoriasis on the other hand are believed to be driven by mutually antagonistic T-cell subsets.

OBJECTIVE

To characterize AA-specific T-cell profiles and inflammatory pattern by intra-individual comparison of AA and coexistent ISD.

METHODS

112 patients with AA were recruited and investigated for coexisting ISD. In-depth analyses were performed in patients with AA and AE (n = 2), AA and psoriasis (n = 1), AA and psoriasis and AE (n = 1) and AA and lichen planus (n = 1), using histology, immunohistochemistry and cytokine staining of T cells isolated from lesional skin.

RESULTS

Of 112 AA patients investigated, 23 suffered from an ISD. The prevalence of AE, vitiligo, psoriasis and lichen planus was higher in the investigated AA cohort than in the normal population. The clinical as well as histological phenotype of AA the coexistent ISD were unequivocal. In line with this, T-cell infiltrates were found to be disease-characteristics with AA and lichen planus dominated by CD8+ and IFN-γ+ TNF-α+ producing T cells while psoriasis lesions in the same patients were dominated by IL-17+ and AE by IL-4+ T cells.

CONCLUSION

AA patients have a higher incidence of various T-cell-driven inflammatory skin diseases than the normal population, a phenomenon which might relate to over-activation of skin-homing T cells and to specific immune triggers as the primary cause of inflammation. More importantly, we showed that by using AA as a model disease, our approach of intra-individual comparison of distinct inflammatory responses in the same patient is feasible and offers the unique possibility to gain insights into disease pathogenesis independent from genetic susceptibilities.

Authors+Show Affiliations

Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.ZAUM - Center of Allergy and Environment, Technical University of Munich and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.ZAUM - Center of Allergy and Environment, Technical University of Munich and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.ZAUM - Center of Allergy and Environment, Technical University of Munich and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.ZAUM - Center of Allergy and Environment, Technical University of Munich and Helmholtz Center Munich, Member of the German Center for Lung Research (DZL), Munich, Germany.Department of Dermatology and Allergy, Technical University of Munich, Munich, Germany.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26416203

Citation

Garzorz, N, et al. "Dissecting Susceptibility From Exogenous Triggers: the Model of Alopecia Areata and Associated Inflammatory Skin Diseases." Journal of the European Academy of Dermatology and Venereology : JEADV, vol. 29, no. 12, 2015, pp. 2429-35.
Garzorz N, Alsisi M, Todorova A, et al. Dissecting susceptibility from exogenous triggers: the model of alopecia areata and associated inflammatory skin diseases. J Eur Acad Dermatol Venereol. 2015;29(12):2429-35.
Garzorz, N., Alsisi, M., Todorova, A., Atenhan, A., Thomas, J., Lauffer, F., Ring, J., Schmidt-Weber, C., Biedermann, T., Eyerich, S., & Eyerich, K. (2015). Dissecting susceptibility from exogenous triggers: the model of alopecia areata and associated inflammatory skin diseases. Journal of the European Academy of Dermatology and Venereology : JEADV, 29(12), 2429-35. https://doi.org/10.1111/jdv.13325
Garzorz N, et al. Dissecting Susceptibility From Exogenous Triggers: the Model of Alopecia Areata and Associated Inflammatory Skin Diseases. J Eur Acad Dermatol Venereol. 2015;29(12):2429-35. PubMed PMID: 26416203.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Dissecting susceptibility from exogenous triggers: the model of alopecia areata and associated inflammatory skin diseases. AU - Garzorz,N, AU - Alsisi,M, AU - Todorova,A, AU - Atenhan,A, AU - Thomas,J, AU - Lauffer,F, AU - Ring,J, AU - Schmidt-Weber,C, AU - Biedermann,T, AU - Eyerich,S, AU - Eyerich,K, Y1 - 2015/09/28/ PY - 2015/03/05/received PY - 2015/07/02/accepted PY - 2015/9/30/entrez PY - 2015/9/30/pubmed PY - 2016/10/16/medline SP - 2429 EP - 35 JF - Journal of the European Academy of Dermatology and Venereology : JEADV JO - J Eur Acad Dermatol Venereol VL - 29 IS - 12 N2 - BACKGROUND: Alopecia areata (AA) is a T-cell-driven autoimmune disease of the hair follicle and frequently reported to be associated with inflammatory skin diseases (ISD) such as atopic eczema (AE) or psoriasis. Interestingly, AA on the one hand and both AE and psoriasis on the other hand are believed to be driven by mutually antagonistic T-cell subsets. OBJECTIVE: To characterize AA-specific T-cell profiles and inflammatory pattern by intra-individual comparison of AA and coexistent ISD. METHODS: 112 patients with AA were recruited and investigated for coexisting ISD. In-depth analyses were performed in patients with AA and AE (n = 2), AA and psoriasis (n = 1), AA and psoriasis and AE (n = 1) and AA and lichen planus (n = 1), using histology, immunohistochemistry and cytokine staining of T cells isolated from lesional skin. RESULTS: Of 112 AA patients investigated, 23 suffered from an ISD. The prevalence of AE, vitiligo, psoriasis and lichen planus was higher in the investigated AA cohort than in the normal population. The clinical as well as histological phenotype of AA the coexistent ISD were unequivocal. In line with this, T-cell infiltrates were found to be disease-characteristics with AA and lichen planus dominated by CD8+ and IFN-γ+ TNF-α+ producing T cells while psoriasis lesions in the same patients were dominated by IL-17+ and AE by IL-4+ T cells. CONCLUSION: AA patients have a higher incidence of various T-cell-driven inflammatory skin diseases than the normal population, a phenomenon which might relate to over-activation of skin-homing T cells and to specific immune triggers as the primary cause of inflammation. More importantly, we showed that by using AA as a model disease, our approach of intra-individual comparison of distinct inflammatory responses in the same patient is feasible and offers the unique possibility to gain insights into disease pathogenesis independent from genetic susceptibilities. SN - 1468-3083 UR - https://www.unboundmedicine.com/medline/citation/26416203/Dissecting_susceptibility_from_exogenous_triggers:_the_model_of_alopecia_areata_and_associated_inflammatory_skin_diseases_ L2 - https://doi.org/10.1111/jdv.13325 DB - PRIME DP - Unbound Medicine ER -