Turning immune-cold tumors hot by targeting the immune checkpoint molecule B7-H4
Treating immune-cold tumors using immunotherapy approach has proved to be a challenge. Recently, Prof. Hongchun Li and his collaborators from the Northwestern University in Chicago, Illinois reported that expression of the immune checkpoint molecule B7-H4 is prevalent among immune-cold triple-negative breast cancers (TNBC), where its expression inversely correlates with that of PD-L1. They turned immune-cold TNBC tumors into immune-hot tumors by targeting the immunosuppressive molecule B7-H4. The protein-protein interactions between B7-H4 and its binding partners as well as the protein stabilities were studied using both experimental and computational approaches. This work has been published in Cancer Discovery entitled "Pharmacologic Suppression of B7-H4 Glycosylation Restores Antitumor Immunity in Immune-Cold Breast Cancers". The full text can be found here.
