Mouse CTLA-4 (Cytotoxic T-Lymphocyte–Associated Protein 4, also known as CD152) is an immune checkpoint receptor belonging to the immunoglobulin superfamily that functions as a critical negative regulator of T-cell activation in mice (Mus musculus). CTLA-4 is primarily expressed on activated CD4⁺ and CD8⁺ T lymphocytes and 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 suppress T-cell proliferation, cytokine production, and immune activation, thereby maintaining immune homeostasis and peripheral tolerance. Mouse CTLA-4 has been extensively studied using genetic knockout models, where CTLA-4–deficient mice develop severe lymphoproliferative disease and fatal systemic autoimmunity, demonstrating the essential role of CTLA-4 in controlling T-cell activation. Because of these findings, mouse models have been fundamental for understanding immune checkpoint biology and for the development of CTLA-4–targeting cancer immunotherapies, including therapies such as ipilimumab, which enhance antitumor immune responses by blocking CTLA-4–mediated inhibitory signaling.