CD200R signaling contributes to unfavorable tumor microenvironment through regulating production of chemokines by tumor-associated myeloid cells.

ABSTRACT: CD200 is overexpressed in many solid tumors and considered as an immune checkpoint molecule dampening cancer immunity. In this study, we found that CD200R^-/- mice were significantly more potent in rejecting these CD200⁺ tumors. scRNA sequencing demonstrated that tumors from CD200R^-/- mice had more infiltration of CD4⁺ and CD8⁺ T cells, and NK cells but less infiltration of neutrophils. Antibody depletion experiments revealed that immune effector cells are crucial in inhibiting tumor growth in CD200R^-/- mice. Mechanistically, we found that CD200R signaling regulates the expression of chemokines in tumor-associated myeloid cells (TAMCs). In the absence of CD200R, TAMCs increased expression of CCL24 and resulted in increased in

SUBMITTER: Lin CH 

PROVIDER: S-EPMC10239067 | biostudies-literature | 2023 Jun

REPOSITORIES: biostudies-literature