CTLA-4 (E2V1Z) Rabbit mAb recognizes endogenous levels of total CTLA-4 protein. Non-specific staining was observed in mouse and human normal and neoplastic liver, in human normal kidney, and in mouse stomach crypts.

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Gln216 of human CTLA-4 protein.

Cytotoxic T-lymphocyte protein 4 (CTLA-4, CD152) is an Ig superfamily member that negatively regulates early T cell activation (1-4). The CTLA-4 protein is primarily expressed on T cells, including CD8⁺ cytotoxic T cells, CD4⁺ helper T cells, and CD4⁺/FoxP3⁺ regulatory T cells (1,2). CTLA-4 protein competes with CD28 for B7.1 (CD80) and B7.2 (CD86) binding at the cell surface, which results in the downregulation of T cell activity (5). The activation of SHP-2 and PP2A downstream of CTLA-4 attenuates TCR signaling (6). Research studies indicate that CTLA4 knockout mice display lymphoproliferative disorders leading to early death, confirming the role of CTLA-4 as a negative regulator of T cells (7). Mutations in the corresponding CTLA4 gene are associated with multiple disorders, including insulin-dependent diabetes mellitus, Graves' disease, Hashimoto thyroiditis, celiac disease, systemic lupus erythematosus, and type V autoimmune lymphoproliferative syndrome (8,9). Additional studies demonstrate that CTLA-4 blockade is an effective strategy for tumor immunotherapy (10-12).