Blood endotyping distinguishes the profile of vitiligo from other inflammatory and autoimmune skin diseases

Publication date: Available online 18 December 2018

Source: Journal of Allergy and Clinical Immunology

Author(s): Tali Czarnowicki, Helen Y. He, Alexandra Leonard, Hyun Je Kim, Naoya Kameyama, Ana B. Pavel, Randall Li, Yeriel Estrada, Huei-Chi Wen, Grace W. Kimmel, Hee J. Kim, Margot Chima, Mark Lebwohl, James G. Krueger, Emma Guttman-Yassky

Abstract

Background

Peripheral blood skin-homing/cutaneous lymphocyte antigen/CLA⁺ T-cells emerge as biomarkers of cutaneous immune activation in inflammatory skin diseases (atopic dermatitis/AD, alopecia areata/AA). However, blood phenotyping across these subsets is not yet available in vitiligo.

Objective

To measure cytokine production by circulating skin-homing (CLA⁺) versus systemic (CLA^-) "polar" CD4⁺/CD8⁺ and activated T-cell subsets in vitiligo compared to AA, AD, psoriasis and controls.

Methods

Flow cytometry was used to measure IFN-γ/IL-13/IL-9/IL-17/IL-22 cytokines in CD4⁺/CD8⁺ T-cells in blood of 19 moderate-to-severe non-segmental/generalized vitiligo patients, moderate-to-severe AA (n=32), psoriasis (n=24), AD (n=43) and controls (n=30). Unsupervised clustering differentiated subjects into groups based on cellular frequencies.

Results

Vitiligo showed the highest CLA⁺/CLA^- Th1/Tc1 polarization with parallel Th2/Th9/Th17/Th22 elevations to levels often higher than AA, AD and psoriasis (P<0.05). Total Tregs were lower in vitiligo than controls, AD, and psoriasis (P<0.001). Vitiligo severity correlated with multiple cytokines (P<0.1), while duration was linked with IFN-γ and IL-17 (P<0.04). Patients and controls grouped into separate clusters based on blood biomarkers.

Conclusions

Vitiligo is characterized by a multi-cytokine polarization among circulating skin-homing and systemic subsets, which differentiates it from other inflammatory/autoimmune skin diseases. Future targeted therapies should delineate the relative contribution of each cytokine axis to disease perpetuation.

Graphical abstract

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