CTLA-4

CTLA-4 (cytotoxic T-lymphocyte-associated protein 4) is an inhibitory immune checkpoint receptor and marker that helps regulate immune homeostasis by dampening T-cell activation. It is a therapeutic target in cancer immunotherapy, where ipilimumab, cadonilimab, and broader immune checkpoint inhibitors act on CTLA-4, and it is also being explored in agonistic-antibody strategies to promote immune tolerance. In the provided data, CTLA-4 expression was correlated with prkd3 expression, linking this checkpoint to broader immunologic and molecular programs. Recent studies also place CTLA-4 in combination strategies, including cordycepin-enhanced blockade and triple-therapy approaches, and in disease contexts such as colorectal and esophageal cancer. Overall, CTLA-4 functions as a central inhibitory node in antitumor immunity, with both blockade and receptor-agonism approaches under active investigation.

Cancer

  • CTLA-4 is discussed as a therapeutic target in colorectal cancer, reflecting its role in checkpoint-based cancer treatment. (PMID:41925220)
  • In colon cancer, CTLA-4 blockade efficacy was enhanced by cordycepin-mediated immunomodulation, suggesting a combination strategy to boost antitumor activity. (PMID:41722537)
  • CTLA-4 was cited among early immune checkpoint targets in esophageal cancer immunotherapy research, indicating its established place in the field. (PMID:41722038)
  • A cancer immunotherapy strategy described CTLA-4 as the target of ipilimumab, and another study context noted targeting by immune checkpoint inhibitors. (PMID:41975460, PMID:42026803)
  • Cadonilimab was described as a dual checkpoint inhibitor targeting CTLA-4, with a study protocol in unresectable or potentially resectable hepatocellular carcinoma. (PMID:41954707)

Immune regulation and molecular associations

  • CTLA-4 is an inhibitory receptor critical for immune homeostasis and is being explored as a target for agonistic antibodies to promote immune tolerance. (PMID:41915422)
  • CTLA-4 expression correlated with prkd3 expression in a pan-cancer multi-omics analysis, linking checkpoint biology with kinase-associated molecular programs. (PMID:41931575)
  • The literature frames CTLA-4 as an immune checkpoint molecule whose modulation can either suppress or enhance immune responses depending on therapeutic design. (PMID:41915422, PMID:41931575)