IL-22–producing “T22” T cells account for upregulated IL-22 in atopic dermatitis despite reduced IL-17–producing TH 17 T cells

• Published in: Journal of allergy and clinical immunology 2009, Vol.123 (6), p.1244-1252.e2
• Main Authors: Nograles, Kristine E., MD, Zaba, Lisa C., PhD, Shemer, Avner, MD, Fuentes-Duculan, Judilyn, MD, Cardinale, Irma, MSc, Kikuchi, Toyoko, MSc, Ramon, Michal, MD, Bergman, Reuven, MD, Krueger, James G., MD, PhD, Guttman-Yassky, Emma, MD, MSc
• Format: Article
• Language: English
• Subjects: Allergy and Immunology
• ISSN: 0091-6749
• DOI: 10.1016/j.jaci.2009.03.041

Background Psoriasis and atopic dermatitis (AD) are common inflammatory skin diseases. An upregulated TH 17/IL-23 pathway was demonstrated in psoriasis. Although potential involvement of TH 17 T cells in AD was suggested during acute disease, the role of these cells in chronic AD remains unclear. Objective To examine differences in IL-23/TH 17 signal between these diseases and establish relative frequencies of T-cell subsets in AD. Methods Skin biopsies and peripheral blood were collected from patients with chronic AD (n = 12) and psoriasis (n = 13). Relative frequencies of CD4+ and CD8+ T-cell subsets within these 2 compartments were examined by intracellular cytokine staining and flow cytometry. Results In peripheral blood, no significant difference was found in percentages of different T-cell subsets between these diseases. In contrast, psoriatic skin had significantly increased frequencies of TH 1 and TH 17 T cells compared with AD, whereas TH 2 T cells were significantly elevated in AD. Distinct IL-22–producing CD4+ and CD8+ T-cell populations were significantly increased in AD skin compared with psoriasis. IL-22+ CD8+ T-cell frequency correlated with AD disease severity. Conclusion Our data established that T cells could independently express IL-22 even with low expression levels of IL-17. This argues for a functional specialization of T cells such that “T17” and “T22” T-cells may drive different features of epidermal pathology in inflammatory skin diseases, including induction of antimicrobial peptides for “T17” T cells and epidermal hyperplasia for “T22” T-cells. Given the clinical correlation with disease severity, further characterization of “T22” T cells is warranted, and may have future therapeutic implications.