The binding of PD-L1 to CD80 on antigen-presenting cells prevents PD-1 ligation on T cells. Therapeutic blockade of the cis-PD-L1–CD80 interaction liberates PD-L1 to bind to PD-1, inhibits autoreactive T cells and robustly alleviates autoimmune symptoms.
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Acknowledgements
This work was supported by the National Institutes of Health (grants R35 CA263850, P01 AI108545, R01s DK089125, AI144422 & AI129893 to D.A.A.V., F31 AI147638 and T32 AI089443 to S.G, F32 CA247004 and T32 CA082084 to A.M.G.D.)
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D.A.A.V. declares competing financial interests and has submitted patents covering LAG3 that are licensed or pending and is entitled to a share in net income generated from licensing of these patent rights for commercial development. D.A.A.V.: cofounder and stock holder of Novasenta, Potenza, Tizona, Trishula; stock holder of Oncorus, Werewolf, Apeximmune; patents licensed and royalties for Astellas, BMS, Novasenta; scientific advisory board member of Tizona, Werewolf, F-Star, Bicara, Apeximmune; consultant for Astellas, BMS, Almirall, Incyte, G1 Therapeutics; research funding from BMS, Astellas and Novasenta.
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Grebinoski, S., Gocher-Demske, A.M. & Vignali, D.A.A. Catch and release: freeing up PD-L1 ameliorates autoimmunity. Nat Immunol 23, 344–346 (2022). https://doi.org/10.1038/s41590-022-01140-2
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DOI: https://doi.org/10.1038/s41590-022-01140-2
