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The Freeman Laboratory studies the contribution of costimulatory signals to the immune response. Following the discovery of PD-L1 and PD-L2 as the ligands for the PD-1 receptor on T cells, we demonstrated the inhibitory function of PD-L1 and PD-L2 on T cells and showed that blockade of this pathway enhanced T cell activation, proliferation, and cytokine production. Further studies showed that PD-L1 is highly expressed by many solid tumors/hematological malignancies, and that blockade of PD-L1 enhances killing of PD-L1 positive targets by CD8 T cells. Recently, PD-1 blocking antibodies were approved by the FDA for the treatment of melanoma and lung cancer.
Our group also discovered the B7-1 and B7-2 molecules that bind to the costimulatory CD28 and coinhibitory CTLA-4 receptor and provide the critical costimulatory signal for full T cell activation, clonal expansion, and development of effector function through their interaction with CD28 on T cells. Following T cell activation, the B7-1–B7-2 interaction with CTLA-4, expressed on activated T cells, leads to down-regulation of T cell activation, whereas stimulation of the TCR alone leads to T cell clonal anergy. Thus, blockade of B7-1 and B7-2 can be used to establish antigen-specific tolerance for transplantation or the alleviation of autoimmunity.
Conversely, B7-1/B7-2 expression can stimulate an immune response, and the introduction of B7-1 or B7-2 into tumors can stimulate an anti-tumor response leading to tumor rejection and anti-tumor immunity. Recently, we have cloned two novel members of the B7 gene family, which bind to receptors expressed on activated T cells and further regulate the development of an immune response. Current studies focus on the function of these novel B7 genes and their interactions with the B7/CD28-CTLA-4 pathway.
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