CTLA4 Antibody

Cytotoxic T-Lymphocyte Associated Antigen-4 (CTLA-4), also known as CD152, is a protein receptor that plays a crucial role in the regulation of immune responses. It functions as an immune checkpoint and is primarily involved in downregulating immune responses .

CTLA-4 is a member of the immunoglobulin superfamily and is structurally similar to the co-stimulatory protein CD28. Both CTLA-4 and CD28 bind to the same ligands, CD80 (B7-1) and CD86 (B7-2), on antigen-presenting cells (APCs). However, while CD28 provides a stimulatory signal to T cells, CTLA-4 delivers an inhibitory signal .

CTLA-4 is constitutively expressed in regulatory T cells (Tregs) and is upregulated in conventional T cells upon activation. This upregulation is particularly notable in the context of cancer, where CTLA-4 acts as an “off” switch when bound to CD80 or CD86, thereby inhibiting T cell activation and proliferation .

The role of CTLA-4 in immune regulation has significant clinical implications. Its ability to downregulate immune responses makes it a target for therapeutic interventions in autoimmune diseases and cancer. For instance, blocking CTLA-4 can enhance T cell activation and is used in cancer immunotherapy to boost the immune system’s ability to fight tumors .

Conversely, agonists of CTLA-4 are being explored for their potential to treat autoimmune diseases by reducing excessive immune activity. The deletion of CTLA-4 in mice has been shown to cause severe autoimmune diseases, highlighting its importance in maintaining immune homeostasis .

Mouse anti-human CTLA-4 antibodies are monoclonal antibodies developed in mice that specifically target the human CTLA-4 protein. These antibodies are used in research and clinical settings to study the function of CTLA-4 and to develop therapeutic strategies. One such therapeutic antibody is Ipilimumab, which is used in the treatment of melanoma and other cancers .

Research on CTLA-4 has expanded our understanding of immune checkpoints and their role in immune regulation. Studies have shown that CTLA-4-Ig (a fusion protein combining the extracellular domain of CTLA-4 with the Fc portion of IgG1) can suppress the expression of CD80, CD86, and pro-inflammatory cytokines in human B cells, thereby limiting T cell activation .

In autoimmune diseases such as rheumatoid arthritis, CTLA-4-Ig (abatacept) has been shown to obstruct CD80/CD86 on the surface of memory B cells, reducing disease activity and improving clinical outcomes .