Expression of CD127 Suppresses T Regulatory Cells in Psoriasis

Abstract

Background: Psoriasis is a genetically regulated autoimmune skin disease associated with the impaired suppressive function of Treg cells. Foxp3 is the accepted marker of Treg cell, but CD127 (IL-7Rα), a surface marker of activated T cell, can distinguish the functional status of CD4+CD25+FoxP3+Treg cells. The study aimed to demonstrate the functional status of Treg cells in peripheral blood of psoriasis patients, to analyze their association with disease severity and duration, serum IL-17 level, and IL-23R gene polymorphism to observe the relationship with susceptibility to psoriasis. Methods: Thirty-five psoriasis patients and 35 healthy controls were enrolled. Demographical details were recorded, severity was assessed by Psoriasis Area and Severity Index (PASI) scoring. Treg cells were quantified by flowcytometric immunophenotyping, serum IL-17 level by ELISA, and IL-23R gene polymorphism by Real-Time PCR. Results: Increased circulatory CD4+CD25+FoxP3+Treg and CD4+CD25+FoxP3+CD127+/pTreg cells observed in psoriatics than in controls (P<0.05) but CD4+CD25+FoxP3+CD127-/tTreg cells significantly decreased (P<0.001). IL-17 levels were elevated in psoriatics (P=0.002). In severe patients, FoxP3 expression decreases in tTreg cells and are CD127+. Out of 35 patients, 23 (65.71%) had an AA genotype of IL23Rrs10889677 gene polymorphism, associated with increased Treg, tTreg, pTreg cells, and IL-17 levels revealed susceptibility to psoriasis. Conclusion: This study shows the loss of tTreg function and pTreg cell activation in psoriasis, supporting the autoimmune disease model. CD127 expression can better distinguish Treg cells and augmenting the CD127-/low population of Treg cells to restore suppressive activity by anti-CD127 mAb therapy can be a potential treatment option for psoriasis patients.