immune cells are also able to kill pathogens by binding to them and engulfing them in a process known as phagocytosis. in macrophages trpv2 recruitment toward the phagosome is regulated by pi3k signaling, protein kinase c, akt kinase, and src kinases. they are able to locate these microbes through chemotaxis which is trpv2 mediated. when the pathogen is endocytosed it is degraded then presented on the membrane of antigen presenting cells (i.e macrophages). macrophages present these antigens to t cells via a major histocompatibility complex (mhc). the region between the mhc-peptide and the t cell receptor is known as the immunosynapse. trpv2 channels are highly concentrated in this region. when these two cells interact, it allows calcium to diffuse through the trpv2 channel. trpv2 mrna has been detected in cd4+ and cd8+ t cells as well as in human b lymphocytes. trpv2 is one type of ion channel that directs t cell activation, proliferation, and defense mechanisms. if the trpv2 channel were absent or not functioning properly in t cells, t cell receptor signaling would not be optimal. trpv2 also acts as a transmembrane protein on the surface of b cells, negatively controlling b cell activation. abnormal trpv2 expression has been reported in hematological diseases including multiple myeloma, myelodysplastic syndrome, burkitt lymphoma, and acute myeloid leukemia.