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pd-l1 and pd-l2 regulate self-tolerance and the immune response to transplants in a nonredundant fashion. to investigate the role of pd-l1 and pd-l2 in tolerance induction, pd-l1/pd-l2/ n4 nod mice received allogeneic islet transplants from balb/c donors and were monitored for t cell responses, survival, and graft function. pd-l1/pd-l2/ n4 nod mice had a markedly accelerated rate of allograft rejection as compared with wt n4 nod mice (p = 0.0008; log-rank test; fig. 1 c). histologically, allografts in pd-l1/pd-l2/ n4 mice were rejected as early as 10 d posttransplant and displayed a phenotype of complete insulitis (inflammation in all of the islets) and intra-islet infiltration of t cells. in contrast, balb/c islet transplants in wt n4 nod mice were rejected later and were associated with a phenotype of immune rejection with scattered insulitis, but the islets were not completely destroyed ( fig. the survival of pd-l1/pd-l2/ n4 nod mice was also significantly shorter than that of wt n4 nod mice after islet transplantation (p = 0.0005; fig. 1 b).
we have now found that pd-l1 and pd-l2 are expressed in a coordinated manner on the same apcs, which suggests a role for these ligands in controlling the function of t cells. however, pd-l1 and pd-l2 appear to control different aspects of t cell tolerance because pd-l1 is expressed on most islet cells whereas pd-l2 is expressed on a subpopulation of islet cells, on the endothelium, and on other cell types, including hematopoietic cells and cells in the brain. the coordinated expression of pd-l1 and pd-l2 on specific cell types provides a mechanism to control t cell responses in a precise manner and prevents aberrant t cell responses against self-antigens. we found that specific deletion of pd-l1 and pd-l2 on hematopoietic cells, on endothelium, or on all cells results in a similar rapid onset of diabetes, suggesting that pd-l1 and pd-l2 are required on all cell types to regulate diabetes. we tested whether a single hematopoietic cell type was sufficient for diabetes development. deletion of pd-l1 and pd-l2 on cd11c+ dcs resulted in an earlier onset of diabetes in nod mice compared to mice with a single deletion of either pd-l1 or pd-l2. this result is consistent with the hypothesis that pd-l1 and pd-l2 are required in multiple cell types, but the results do not rule out a role for other cell types. these studies are supported by the observation that pd-l1 and pd-l2 are expressed on islet cells. it is possible that other cells within the islets express a ligand for pd-l1 and pd-l2 that provides a path for t cell entry. however, the fact that the deletion of pd-l1 and pd-l2 on all cells, cd11c+ dcs, and endothelium all result in similar accelerated diabetes onset suggests that the pd-l1 and pd-l2 pathways are not redundant. indeed, our studies have shown that the pd-l1 and pd-l2 pathways function independently in controlling t cell responses. furthermore, the data suggest that the pd-l1 and pd-l2 pathways are highly conserved and function independently within the islets, potentially in other target organs.
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