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TIGIT expression levels on CD 4+ T cells are correlated with disease severity in patients with psoriasis
Author(s) -
Wang F. F.,
Wang Y.,
Wang L.,
Wang T. S.,
Bai Y. P.
Publication year - 2018
Publication title -
clinical and experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.587
H-Index - 78
eISSN - 1365-2230
pISSN - 0307-6938
DOI - 10.1111/ced.13414
Subject(s) - tigit , t cell , flow cytometry , psoriasis , psoriasis area and severity index , interleukin 17 , immunology , medicine , endocrinology , cytokine , immune system
Summary Background T‐cell immunoglobulin and ITIM domain ( TIGIT ), a co‐inhibitory receptor, suppresses CD 4+ T‐cell responses by triggering CD 155. TIGIT shifts the balance of cytokines, including interferon ( IFN )‐γ, interleukin ( IL )‐10 and IL ‐17A, and affects the proliferation of CD 4+ T cells. Aim To investigate TIGIT expression and its effects on CD 4+ T‐cell function in psoriasis. Methods In total, 28 patients with psoriasis vulgaris PV and 14 healthy controls ( HC s) were enrolled. TIGIT expression on CD 4+ T cells was evaluated by flow cytometry analysis and quantitative real‐time PCR . Production of IFN ‐γ, IL ‐10 and IL ‐17 was measured with cytometry bead arrays, while CD 4+ T cell proliferation was measured using a permeable assay. Results IGIT expression on CD 4+ T cells and mRNA level were significantly lower in patients with PV compared with HC s. TIGIT expression was negatively correlated with Psoriasis Area and Severity Index. Activation of TIGIT with recombinant human CD 155/Fc protein significantly inhibited psoriatic CD 4+ T‐cell proliferation, decreased production of IFN ‐γ and IL ‐17A, and increased IL ‐10. After blockade with a functional anti‐human TIGIT antibody, TIGIT produced the opposite effect on IFN ‐γ and IL ‐17A, but had no significant effect on IL ‐10 or cell proliferation. Furthermore, the frequency of TIGIT + CD 4+ T cells was significantly increased in patients with PV after 2 months of treatment with acitretin, with associated significant changes in IFN ‐γ, IL ‐10and IL ‐17A plasma levels. Conclusions Downregulation of TIGIT on CD 4+ T cells may contribute to the pathogenesis of psoriasis, and activation of the TIGIT signalling pathway may be a potential therapeutic target.