Human CTLA-4 (Cytotoxic T-Lymphocyte–Associated Protein 4, also known as CD152) is an immune checkpoint receptor belonging to the immunoglobulin superfamily that plays a critical role in the negative regulation of T-cell activation and maintenance of immune tolerance. CTLA-4 is primarily expressed on activated CD4⁺ and CD8⁺ T lymphocytes and constitutively on regulatory T cells (Tregs) following antigen stimulation. It binds to the costimulatory ligands CD80 (B7-1) and CD86 (B7-2) on antigen-presenting cells such as dendritic cells, macrophages, and B cells, competing with the activating receptor CD28 for these ligands. Engagement of CTLA-4 transmits inhibitory signals that reduce T-cell proliferation, cytokine production, and immune activation, thereby maintaining immune homeostasis and preventing excessive or autoimmune immune responses. Dysregulation of CTLA-4 signaling has been associated with autoimmune diseases, chronic inflammatory disorders, and cancer immune evasion. CTLA-4 is also a major target in cancer immunotherapy, where checkpoint inhibitor antibodies such as ipilimumab block CTLA-4 signaling to enhance T-cell–mediated antitumor immunity, making CTLA-4 a central focus in immunology, oncology, and therapeutic development.