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- W4383559852 abstract "Abstract Complement factor H (CFH) is an abundant serum protein regulating complement activation and protecting host cells from attack by the alternative pathway of complement mediated cytotoxicity. We previously identified an anti-CFH autoantibody in early-stage NSCLC patients, and cloned from single peripheral B cells a lead therapeutic mAb, GT103, for cancer immunotherapy. Although GT103 has potent antitumor activities, the underlying mechanisms remain unknown. Herein we investigated GT103-mediated antitumor effects and demonstrate that murine GT103 (mGT103) enhances antitumor immunity through multiple pathways. It creates a favorable tumor microenvironment (TME) by decreasing immunosuppressive regulatory T cells and myeloid-derived suppressor cells and enhancing antigen-specific effector T cells, and has a synergistic antitumor effect with anti-PD-L1 mAb. mGT103, previously shown to activate complement in vitro and in vivo, requires complement for its activity in vivo. Furthermore, the immune landscape of tumors from early-stage patients expressing the anti-CFH autoantibody is associated with an immunologically active TME. Our results provide novel mechanistic insights into this promising human-derived immunotherapeutic agent, which is currently undergoing a phase Ib clinical trial as monotherapy and a phase II combination trial with Keytruda for advanced, refractory/relapsed NSCLC patients." @default.
- W4383559852 created "2023-07-08" @default.
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- W4383559852 date "2023-07-07" @default.
- W4383559852 modified "2023-10-18" @default.
- W4383559852 title "Creation of a Favorable Antitumor Microenvironment by the Anti-Complement Factor H Antibody mGT103" @default.
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- W4383559852 doi "https://doi.org/10.21203/rs.3.rs-2001920/v2" @default.
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