Cytotoxic T-Lymphocyte-Associated Protein 4 (CTLA-4) has a molecular weight of approximately 33-34 kDa and is primarily expressed on activated T-cells, specifically CD4+ and CD8+ T-cells. It is a crucial immune checkpoint receptor that negatively regulates T-cell activation. It competes with the co-stimulatory molecule CD28 for binding to the ligands B7-1 (CD80) and B7-2 (CD86) on antigen-presenting cells (APCs), which inhibits T-cell activation and helps maintain immune homeostasis.

CTLA-4 is associated with autoimmune diseases, as its dysregulation can lead to an overactive immune response against self-antigens. Additionally, mutations in Cytotoxic T-Lymphocyte-Associated Protein 4 are linked to certain autoimmune disorders, such as systemic lupus erythematosus (SLE) and autoimmune thyroid diseases. Furthermore, it is a target in cancer immunotherapy due to its role in immune evasion by tumor cells.

Therapeutically, antibodies against CTLA-4 have been shown to block the CTLA-4 inhibitory function, promoting T-cell activation and enhancing the immune response against cancer cells, particularly in treating advanced melanoma. In diagnostics, assessing CTLA-4 expression or genetic variations may help predict responses to immunotherapy and guide treatment decisions.