BTLA

BTLA (B and T Lymphocyte Attenuator), also known as BTNL9 or BTLA, is an immune checkpoint molecule primarily expressed on T cells, B cells, and NK cells. It is encoded by a gene within the human genome. The mechanism of action of BTLA involves binding to its specific ligand HVEM (Herpesvirus Entry Mediator), which inhibits the activation, proliferation, and cytokine production of T cells and B cells. Binding of BTLA to HVEM activates immunoreceptor tyrosine-based inhibitory motifs (ITIMs) and immunoglobulin tyrosine switch motifs (ITSMs), leading to the phosphorylation and recruitment of SHP-1 and SHP-2, which in turn inhibits T cell proliferation and IL-2 production, resulting in an immunosuppressive effect.

BTLA is involved in the regulation of multiple physiological and pathological processes, including cancer, inflammatory diseases, and autoimmune disorders. In the tumor microenvironment, activation of BTLA is one of the potential mechanisms of resistance to PD-1 antibodies, and BTLA expression is closely associated with tumor progression. In inflammatory diseases, BTLA negatively regulates inflammation mediated by T cells. Furthermore, in autoimmune diseases, the level of BTLA expression correlates with disease activity. As such, BTLA is a potential target for immunological research and the treatment of related diseases.