IL17A and neoplasm: Given the polyfunctionality of CD4+CD26high T cells (indicated by their ability to co-express IL-17A, IFNγ, IL-2, TNFα, and Granzyme B), our findings could be the result of enhanced inflammation at the tumor site (i.e., induction of a “hot” tumor), which has been shown to associate with tumor regression51, 52.