February 1, 2005 | Fumiya Hirano, Katsumi Kaneko, Hideto Tamura, Haidong Dong, Shengdian Wang, Masao Ichikawa, Cecilia Rietz, Dallas B. Flies, Julie S. Lau, Gefeng Zhu, Koji Tamada, and Lieping Chen
The study investigates how the expression of B7-H1 and PD-1 on tumor cells can block the immune system's ability to destroy cancer. B7-H1 is a member of the B7 family and is expressed on many cancers. When B7-H1 is present on tumor cells, it can prevent the effectiveness of certain immunotherapies, such as those targeting CD137. This resistance is due to B7-H1's interaction with PD-1 on T cells, which inhibits T cell activity. However, blocking B7-H1 or PD-1 with specific monoclonal antibodies can reverse this resistance and significantly enhance the effectiveness of immunotherapy. The study suggests that B7-H1 and PD-1 form a molecular shield that prevents T cells from attacking tumor cells. This finding highlights the importance of targeting these molecules in cancer immunotherapy to improve treatment outcomes. The research also shows that B7-H1 can be constitutively or inducibly expressed on tumor cells, and its expression can be regulated by IFN-γ. The study provides evidence that blocking B7-H1 or PD-1 can enhance the immune response against tumors, offering new strategies for cancer treatment. The results indicate that B7-H1 and PD-1 play a critical role in tumor immune evasion, and their inhibition could be a promising approach for improving cancer immunotherapy.The study investigates how the expression of B7-H1 and PD-1 on tumor cells can block the immune system's ability to destroy cancer. B7-H1 is a member of the B7 family and is expressed on many cancers. When B7-H1 is present on tumor cells, it can prevent the effectiveness of certain immunotherapies, such as those targeting CD137. This resistance is due to B7-H1's interaction with PD-1 on T cells, which inhibits T cell activity. However, blocking B7-H1 or PD-1 with specific monoclonal antibodies can reverse this resistance and significantly enhance the effectiveness of immunotherapy. The study suggests that B7-H1 and PD-1 form a molecular shield that prevents T cells from attacking tumor cells. This finding highlights the importance of targeting these molecules in cancer immunotherapy to improve treatment outcomes. The research also shows that B7-H1 can be constitutively or inducibly expressed on tumor cells, and its expression can be regulated by IFN-γ. The study provides evidence that blocking B7-H1 or PD-1 can enhance the immune response against tumors, offering new strategies for cancer treatment. The results indicate that B7-H1 and PD-1 play a critical role in tumor immune evasion, and their inhibition could be a promising approach for improving cancer immunotherapy.