Cytotoxic T-lymphocyte protein 4 (CTLA-4) (CTLA-4)

Mouse Cytotoxic T-lymphocyte protein 4 (CTLA-4), also known as CD152, is a critical immune checkpoint receptor primarily expressed on activated T cells and constitutively on regulatory T cells (Tregs) [3, 9]. It belongs to the immunoglobulin superfamily and functions as a potent negative regulator of T-cell immune responses by outcompeting the costimulatory receptor CD28 for binding to B7-1 (CD80) and B7-2 (CD86) ligands on antigen-presenting cells [3, 5]. In preclinical research, mouse CTLA-4 is a primary target for evaluating cancer immunotherapies, where blocking its activity with surrogate antibodies like 9D9 or 9H10 enhances anti-tumor T-cell activation and promotes the depletion of intratumoral Tregs [2, 5]. Conversely, CTLA-4-Ig fusion proteins utilize the high-affinity binding of CTLA-4 to B7 ligands to inhibit T-cell activation, serving as a therapeutic strategy for autoimmune diseases and transplant rejection in murine models [8, 10]. Understanding the biology of mouse CTLA-4 is vital for translating checkpoint inhibition strategies from murine models to human clinical applications.

Other names

CD152Cytotoxic T-lymphocyte-associated antigen 4Ctla-4Ctla4

Competitive inhibition of CD28 costimulation by binding to CD80 and CD86 ligands; depletion of regulatory T cells (Tregs) via antibody-dependent cellular cytotoxicity (ADCC) [2, 4, 5].