Functional redundancy of PI3K isoforms in conventional T cells provides a selective Treg-targeting strategy through inhibition of PI3K-delta isoform

Increased regulatory T cell (Treg) numbers within tumors and circulation of cancer patients, observed in early studies, implied their involvement in pathogenesis and disease progression. Also, Treg increase in cancer patients have been associated with reduced survival and inhibition of anti-tumor immune responses. Therefore, decreasing the numbers and/or function of Tregs is needed to facilitate better outcomes for cancer patients. The phosphoinositide 3-kinase (PI3K-Akt) pathway plays important roles in cell growth, survival, and proliferation of T cells. However, little is known about the role of different isoforms of PI3K in different T subsets activation. Here, we explore the role of PI3K isoforms in Tregs and conventional T cell activation with the intention of identifying potential differences to selectively inhibit Tregs.