Cancer-derived sialylated IgG promotes tumor immune escape by binding to Siglecs on effector T cells.

ABSTRACT: To date, IgG in the tumor microenvironment (TME) has been considered a product of B cells and serves as an antitumor antibody. However, in this study, using a monoclonal antibody against cancer-derived IgG (Cancer-IgG), we found that cancer cells could secrete IgG into the TME. Furthermore, Cancer-IgG, which carries an abnormal sialic acid modification in the CH1 domain, directly inhibited effector T-cell proliferation and significantly promoted tumor growth by reducing CD4⁺ and CD8⁺ T-cell infiltration into tumor tissues. Mechanistic studies showed that the immunosuppressive effect of sialylated Cancer-IgG is dependent on its sialylation and binding to sialic acid-binding immunoglobulin-type lectins (Siglecs) on effector CD4⁺ and CD8⁺ T cells. I

SUBMITTER: Wang Z 

PROVIDER: S-EPMC7784903 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature