|Publication Type||Journal Article|
|Year of Publication||2020|
|Authors||Pauken, KE, Godec, J, Odorizzi, PM, Brown, KE, Yates, KB, Ngiow, SFoong, Burke, KP, Maleri, S, Grande, SM, Francisco, LM, Ali, M-A, Imam, S, Freeman, GJ, W Haining, N, E Wherry, J, Sharpe, AH|
|Date Published||2020 Jun 30|
The PD-1 pathway regulates dysfunctional T cells in chronic infection and cancer, but the role of this pathway during acute infection remains less clear. Here, we demonstrate that PD-1 signals are needed for optimal memory. Mice deficient in the PD-1 pathway exhibit impaired CD8 T cell memory following acute influenza infection, including reduced virus-specific CD8 T cell numbers and compromised recall responses. PD-1 blockade during priming leads to similar differences early post-infection but without the defect in memory formation, suggesting that timing and/or duration of PD-1 blockade could be tailored to modulate host responses. Our studies reveal a role for PD-1 as an integrator of CD8 T cell signals that promotes CD8 T cell memory formation and suggest PD-1 continues to fine-tune CD8 T cells after they migrate into non-lymphoid tissues. These findings have important implications for PD-1-based immunotherapy, in which PD-1 inhibition may influence memory responses in patients.
|Alternate Journal||Cell Rep|
|Grant List||R01 CA229851 / CA / NCI NIH HHS / United States |
U19 AI082630 / AI / NIAID NIH HHS / United States