CTLA-4 is a key immune checkpoint molecule that plays an important role in downregulating immune responses and maintaining self-tolerance. Its modulation has critical implications in cancer immunotherapy.
CTLA-4 is primarily expressed on activated T cells (and constitutively on regulatory T cells), where it functions as a negative regulator of T-cell immune responses.
CTLA-4 has been one of the first immune checkpoint molecules targeted in cancer therapy.
– Blockade of CTLA-4 (e.g., with ipilimumab) can enhance T-cell activation and restore antitumor immunity, leading to durable responses in certain cancer types such as melanoma.
Cancers such as melanoma, NSCLC, RCC, colorectal cancer, HNSCC, and certain hematologic malignancies, elevated CTLA-4 expression—especially on tumor-infiltrating lymphocytes—often correlates with an immunosuppressive, exhausted T-cell phenotype and poorer prognosis. However, this same expression also marks tumors that may respond to CTLA-4 blockade therapies, highlighting its dual role as a prognostic biomarker and a therapeutic target in the rapidly evolving field of cancer immunotherapy.
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