While head and neck squamous cell carcinomas are associated with profound immune suppression, less is known about the immunological milieu of premalignant oral lesions. IL-23 to be a significant contributor to the inflammatory IL-17 phenotype in premalignant oral lesions and suggest the decline in IL-23 in HNSCC leads to a decline in Th17 cells. hallmarks of HNSCC is the profound inhibition of immune competence that is mediated in part by immunosuppressive cell populations including immune inhibitory macrophages, T-cells that are skewed toward a Th2 phenotype, Treg cells, myeloid-derived suppressor cells (MDSC) and the less mature CD34+ progenitor cells. The prominent production of IL-23 by premalignant oral lesion tissues led to the assessment of its contribution to the Th17 cell induction by premalignant oral lesions and the lack of Th17 induction by HNSCC.
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Last date updated on September, 2014