Answer :
T cell failure is a defining trait of both cancer and persistent viral infections. A PD-1+ Tcf-1+ CD8+ T cell subset with the ability to self-renew and differentiate into more terminally differentiated cells that downregulate Tcf-1 and express additional inhibitory molecules like Tim3 has been identified in recent studies of chronic lymphocytic choriomeningitis virus (LCMV) infection.
- Here, we show that this terminally differentiated population is divided into two subgroups by the expression of the glycoprotein CD101.
- Initially differentiating into a transitory population of CD101-Tim3+ cells, stem-like Tcf-1+ CD8+ T cells later transformed into CD101+ Tim3+ cells.
- Recent CD101-Tim3+ cell proliferation in vivo, viral control, and expression of the chemokine receptor CX3CR1, pro-inflammatory cytokines, and granzyme B are all characteristics of these effector-like cells.
- Increased CD101-Tim3+ CD8+ T cell counts in response to PD-1 pathway inhibition raise the possibility that these recently formed transitional cells are essential for PD-1-based immunotherapy.
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