Figure 5.

The role of PD-1 in Treg homeostasis after allogeneic HSCT. PD-1 deficient effector T cells aggressively proliferate after HSCT and produce large amounts of inflammatory cytokines. The highly inflammatory cytokine milieu accelerates the proliferation of PD-1 deficient Tregs, but they cannot maintain proliferation due to their high susceptibility to apoptosis. Unbalanced reconstitution of T-cell subsets results in severe GVHD (A). In contrast, with PTCy intervention, alloreactive proliferative effector T cells are efficiently eliminated, contributing to reduced inflammatory cytokine production. It enables Tregs to restore the appropriate levels of proliferation and maintain homeostasis, which contributes to the prevention of severe GVHD (B). PD-1, programmed cell death 1; Treg, regulatory T cell; Teff, effector T cell; PTCy, post-transplant cyclophosphamide.