Targeting PD-L1-CMTM6 interactions in myeloid cells triggers PD-L1 degradation and enhances cytotoxic T-cell expansion.

ABSTRACT:

Background

Immune checkpoint therapies targeting programmed cell death protein 1 (PD-1) and programmed death ligand 1 (PD-L1) have been met with limited clinical responses in the treatment of patients of varying cancer types. Current US Food and Drug Administration (FDA)-approved therapies function to prevent PD-1 binding to PD-L1, thereby preventing T-cell suppression. However, these therapies fail to prevent PD-L1 intrinsic signaling and recycling, which can render these treatments ineffective. Moreover, most research primarily focuses on how these antibodies affect tumor cells and their interactions with T cells. Myeloid cells, which also express PD-L1 and influence T-cell responses, are integral to the efficacy of these therapies. However, strategies that can target these cells

SUBMITTER: Hsu MA 

PROVIDER: S-EPMC12570910 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature