Seon Hee Chang

TL;DR: In vivo, antibody to IL- 17 inhibited chemokine expression in the brain during experimental autoimmune encephalomyelitis, whereas overexpression of IL-17 in lung epithelium caused Chemokine production and leukocyte infiltration, indicating a unique T helper lineage that regulates tissue inflammation.

TL;DR: A pathway whereby cytokines regulate THi differentiation through a selective STAT transcription factor that functions to regulate lineage-specific gene expression is demonstrated.

TL;DR: It is shown that interleukin-1 (IL-1) signaling on T cells is critically required for the early programming of Th 17 cell lineage and Th17 cell-mediated autoimmunity and this pathway may serve as a unique target for Th17cell-mediated immunopathology.

TL;DR: It is found that the development of Th17 and Foxp3(+) Treg cells was associated in immune responses and molecular antagonism and plasticity of Treg and Th17 cell programs are demonstrated.

TL;DR: IL-17F is an important regulator of inflammatory responses that seems to function differently than IL-17 in immune responses and diseases, and this requires IL- 17 receptor A, tumor necrosis factor receptor–associated factor 6, and Act1.