The Role of Dectin-1 Signaling in Altering Tumor Immune Microenvironment in the Context of Aging.

An increased accumulation of immune-dysfunction-associated CD4Foxp3 regulatory T cells (T) is observed in aging oral mucosa during infection. Here we studied the function of T during oral cancer development in aging mucosa. First, we found heightened proportions of T and myeloid-derived suppressor cells (MDSC) accumulating in mouse and human oral squamous cell carcinoma (OSCC) tissues.

IL-1β-MyD88-mTOR Axis Promotes Immune-Protective IL-17AFoxp3 Cells During Mucosal Infection and Is Dysregulated With Aging.

CD4Foxp3T maintain immune homeostasis, but distinct mechanisms underlying their functional heterogeneity during infections are driven by specific cytokine milieu. Here we show that MyD88 deletion in Foxp3 cells altered their function and resulted in increased fungal burden and immunopathology during oral (CA) challenge. Excessive inflammation due to the absence of MyD88 in T coincided with a reduction of the unique population of IL-17A expressing Foxp3 cells (T17) and an increase in dysfunctional IFN-γ/Foxp3 cells (TIFN-γ) in infected mice.