ScholarWorks@중앙대학교

초록

T helper 17 (Th17) cells are a subset of CD4+ T cells that play crucial roles in both host defense and pathological inflammation. Depending on the cytokine milieu, Th17 cells differentiate into tissue-protective non-pathogenic or inflammation-inducing pathogenic subsets. Recent studies have revealed that Th17 cells possess high plasticity, enabling them to convert into Tr1, Th1, Th2, Tfh, or Treg-like subsets in response to microenvironmental cues. This plasticity is considered a key factor linking Th17 cells to the pathogenesis of various inflammatory and autoimmune diseases. Accordingly, therapeutic approaches have shifted from simply blocking inflammatory cytokines to strategies aimed at restoring immune homeostasis by reprogramming pathogenic Th17 cells toward non-pathogenic or regulatory phenotypes. This review focuses on the plasticity of Th17 cells and discusses how modulation of Th17 cell fate contributes to understanding the immunopathogenesis of chronic inflammatory diseases and the development of novel therapeutic strategies.

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