| First Author | Hudson WH | Year | 2019 |
| Journal | Immunity | Volume | 51 |
| Issue | 6 | Pages | 1043-1058.e4 |
| PubMed ID | 31810882 | Mgi Jnum | J:305827 |
| Mgi Id | MGI:6706564 | Doi | 10.1016/j.immuni.2019.11.002 |
| Citation | Hudson WH, et al. (2019) Proliferating Transitory T Cells with an Effector-like Transcriptional Signature Emerge from PD-1(+) Stem-like CD8(+) T Cells during Chronic Infection. Immunity 51(6):1043-1058.e4 |
| abstractText | T cell dysfunction is a characteristic feature of chronic viral infection and cancer. Recent studies in chronic lymphocytic choriomeningitis virus (LCMV) infection have defined a PD-1(+) Tcf-1(+) CD8(+) T cell subset capable of self-renewal and differentiation into more terminally differentiated cells that downregulate Tcf-1 and express additional inhibitory molecules such as Tim3. Here, we demonstrated that expression of the glycoprotein CD101 divides this terminally differentiated population into two subsets. Stem-like Tcf-1(+) CD8(+) T cells initially differentiated into a transitory population of CD101(-)Tim3(+) cells that later converted into CD101(+) Tim3(+) cells. Recently generated CD101(-)Tim3(+) cells proliferated in vivo, contributed to viral control, and were marked by an effector-like transcriptional signature including expression of the chemokine receptor CX3CR1, pro-inflammatory cytokines, and granzyme B. PD-1 pathway blockade increased the numbers of CD101(-)Tim3(+) CD8(+) T cells, suggesting that these newly generated transitional cells play a critical role in PD-1-based immunotherapy. |
