Citations 2
LAG3 and PD1 co-inhibitory molecules collaborate to limit CD8+ T cell signaling and dampen antitumor immunity in a murine ovarian cancer model
Huang, Ruea-Yea, Eppolito, Cheryl, Lele, Shashikant , Shrikant, Protul, Matsuzaki, Junko , Odunsi, Kunle , Huang, Ruea-Yea
Oncotarget | September 29, 2015 | Volume: 6 | Issue: 29 | Pages: 27359-27377
β-Catenin in dendritic cells exerts opposite functions in cross-priming and maintenance of CD8 + T cells through regulation of IL-10
Fu, Chunmei, Liang, Xinjun , Cui, Weiguo , Ober-Blöbaum, Julia L., Vazzana, Joseph, Shrikant, Protul, Lee, Kelvin P. , Clausen, Björn E. , Jiang, Aimin , Shrikant, Protul A, Mellman, Ira , Cui, Weiguo
Proceedings of the National Academy of Sciences | February 17, 2015 | Volume: 112 | Issue: 9 | Pages: 2823-2828
Significance While CD8 + T cells are essential for antitumor immunity, tumors often evade CD8 + T cell surveillance by immunosuppression. Recent study has shown that tumor-induced β-catenin activation in DCs suppresses CD8 + T cell immunity by inhibiting cross-priming, suggesting that activation of β-catenin in DCs might be a key mechanism tumors use to achieve immunosuppression. This report identified mTOR/IL-10 signaling as a previously unidentified mechanism for β-catenin–dependent inhibition of cross-priming. Surprisingly, our study also revealed that β-catenin in DCs was required for CD8 + T cell maintenance post-clonal expansion, suggesting that β-catenin exerts opposite functions during different stages of CD8 + T cell responses. Based on these findings, we have demonstrated selectively manipulating β-catenin signaling as a feasible strategy to improve DC vaccine efficacy.