| Autor: |
García, Eva-Maria, Galicia-Carreón, Jorge, Novak, Natalija |
| Předmět: |
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| Zdroj: |
International Archives of Allergy & Immunology; 2020, Vol. 181 Issue 5, p353-356, 4p, 2 Graphs |
| Abstrakt: |
Background: Atopic dermatitis (AD) is one of the most common inflammatory skin diseases, with an increasing incidence in clinical practice. AD models have demonstrated that TGF-β signaling is compromised in regulatory T cells (Tregs). Objectives: This study aimed to investigate the TGF-β-dependent in vitro conversion of CD4+CD25– T cells derived from AD-patients into CD4+CD25+Foxp3+ induced Tregs (iTregs) in comparison to healthy controls. Methods: To analyze in vitro iTreg conversion, human CD4+CD25– T cells were cultured on anti-CD3-coated plates in the presence of TGF-β and IL-2 for up to 3 days. Consequently, the underlying mechanism of impaired CD4+CD25+Foxp3+ iTreg generation was explored by focusing on TGF-β signaling. Finally, the functionality of iTregs was investigated. Results: Conversion of CD4+CD25–Foxp3– into CD4+CD25+Foxp3+ iTregs was diminished in AD individuals. Impaired iTreg generation was accompanied by a reduced surface expression of GARP (glycoprotein A repetitions predominant), a marker for activated Tregs. A reduced expression of Smad3 mRNA was revealed in CD4+CD25– T cells. Interestingly, the suppressive quality of iTregs was found to be equal in cells derived from AD and healthy donors. Conclusion: The signaling effect of TGF-β receptors on the suppressor quality of iTreg conversion is conserved. Impaired iTreg generation might be a reason for the lack of immune suppression in AD patients and contributes to the chronicity of the disease. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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