Changes in T-cell subsets and their association with disease severity in patients with alopecia areata

Abstract

Background/aim Alopecia areata (AA) is a nonscarring hair loss disorder characterized by genetic susceptibility, environmental triggers, and T-cell–mediated autoimmunity. While various CD4+ and CD8+ T-cell subsets are implicated in its pathogenesis, the roles of follicular T-cell (Tfh), peripheral T-cell (Tph), and regulatory T-cell (Treg) subsets–particularly within the CD8+ population–remain incompletely defined. This study aimed to characterize circulating CD4+ and CD8+ T-cell subsets in Turkish patients with AA and to evaluate their associations with disease activity, duration, and severity. Materials and methods A total of 40 patients with AA and 40 healthy controls were enrolled. CD4+ and CD8+ T-cell subsets—including Th1, Th2, Th17, Th22, Tc1, Tc2, Tc17, Tc22, Treg, Tfh, and Tph cells—were analyzed by flow cytometry based on surface marker expression and intracellular cytokine profiles. Disease severity was assessed using the Severity of Alopecia Tool (SALT) score, and disease activity was evaluated by the hair pull test. Results Patients with AA exhibited significantly lower frequencies of Tc17 and Tc22 cells than healthy controls. CD4+ Tfh cell levels were positively correlated with disease duration. CD4+ Tregs, resting Tregs, CD3+IL-4+ cells, and Tc2 cells were positively associated with SALT scores, whereas CD4+ and CD8+ Tph cells were inversely associated. CD8+ T-cell populations, CD4+ Treg subsets, CD3+IFN-γ+ cells, Th1 cells, and Th2 cells were associated with disease activity, as assessed by the hair pull test. Conclusion Alopecia areata is associated with alterations in circulating T-cell subsets, particularly Tc17 and Tc22 subsets. Selected cytokine-producing and regulatory T-cell subsets are associated with disease activity. These findings support a heterogeneous and dynamic immune profile in AA and highlight the importance of multivariate approaches in identifying independent immunological correlates. Further studies integrating tissue-level analysis and longitudinal follow-up are needed to clarify the underlying mechanisms.