Third, inflammatory cytokines, including IL-1, IL-6, IL-12, and IFN-γ provide a third signal that acts directly on T cells, referred to as the “danger signal”. This signal was found to optimally activate TH1 differentiation and lead to clonal expansion of T cells.
"Th17 cells and IL-17 participate in antitumor immunity by facilitating T cell recruitment to the tumor site and CD8+ T cell priming and effector differentiation suggests a new avenue for developing Th17 cell-based therapy."
~S. A. Rosenberg~
"Using in vitro and in vivo approaches, we determined that under neutral conditions, simultaneous activation of Tregs and naive CD4+ conventional T cells in the presence of APCs resulted in conversion of Tregs into IL-17–producing cells, and endogenous IL-1β was mandatory in this process" according to Vassiliki A. Boussiotis et al
Thus, the addition of IL-6 and IL-1β to the tumor microenvironment skews the balance toward Th17 cells in a murine model of pancreatic cancer and Melanoma.
So we need to suppress the Tregs and generate Th17 T-cells to initiate the right immune response.
“It is not the strongest of the species that survives, nor the most intelligent, but the one most responsive to change.”
~Charles Darwin~
Take Care,
Jimmy B
No comments:
Post a Comment