B7-H4 Pathway in Islet Transplantation and β-Cell Replacement Therapies

Figure 3

The mechanism of B7-H4 action in islet transplantation. Interaction between B7-H4 and an unknown receptor on activated T cells leads to a series of intracellular signalling cascades that result in improved allograft survival. B7-H4 protects allograft rejection through deletional and nondeletional mechanisms. It can limit cytotoxic CD8⁺ proliferation and transcription of granzyme B. It also reduces the Th1 response which may facilitate generation of suppressive Foxp3⁺ Tregs. The combination of controlling activated T-cell proliferation and promoting regulatory T-cell subsets results in enhanced allograft survival and induction of donor-specific tolerance.