Free Download High Quality Gene Control Latchman 16
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our data reveal that pd-l1 expression on parenchymal cells rather than hematopoietic cells protects against autoimmune diabetes and point to a novel role for pd-1/pd-l1 interactions in mediating tissue tolerance.
as outlined above, current concepts of peripheral tolerance emphasize the importance of immune cell regulation by the t regulatory (treg) cells. interestingly, pd-1 and its ligands, pd-l1 and pd-l2, are expressed by natural killer (nk) cells, treg cells, memory t cells, and in turn, they are targets of treg cell activity. a detailed understanding of the interaction of pd-1 and pd-l1/pd-l2 and their unique contributions to the development of autoimmune and infectious disease, and cancer may have relevance for drug design. for example, therapies that target these receptors may benefit not only autoimmune diseases, but also cancers as well as other immune disorders. in addition, blocking pd-1/pd-l1 interactions may be a therapeutic option in chronic viral infections. finally, targeting the pd-1/pd-l1 axis as a therapy in murine models of infectious diseases has achieved impressive results. while the exact mechanisms by which pd-1/pd-l1 blockade inhibits the pathogenesis of infectious diseases remain unclear, pd-1/pd-l1 interaction may indirectly regulate t cell responses during infections.
the anti-pd-l1 antibody, b7-h3 (b7s3), inhibits the growth of some human breast, pancreatic, and other cancers in mice. the importance of b7-h3 in the pathogenesis of cancer was unknown, so we generated mice lacking b7-h3 and analyzed the tumors that developed in these mice. significantly, tumors from b7-h3-deficient mice grew much more slowly than tumors from control mice (p < 0.02), on average developing pathological readings of 430 mg/dl versus 330 mg/dl (t test, <0.05, p < 0.05), respectively. in addition, mice deficient in b7-h3tumor growth and b7-h3 expression protected against carcinogenesis in different organs, and in an immunodeficiency model, demonstrating importance of b7-h3in driving tumorigenesis. therefore, targeting the b7-h3 pathway may offer therapeutic benefits to a variety of human cancers. b7-h3 (b7s3) is important for the prevention of breast and pancreatic cancers.
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. 5ec8ef588b
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