Trogocytosis - Physiological Consequences of Trogocytosis

Physiological Consequences of Trogocytosis

Trogocytosis can have physiological consequences in two ways : either because "recipient" cells acquire and make use of molecules they do not usually express or because « donor » cells are stripped of molecules, which may alter their interaction with cellular partners. Acquired molecules, such as regulatory molecules with extracellular or intracellular components might alter the lymphocytes activity and direct several lymphocyte functions, such as migration to the adequate injured tissues. Such gained plasma membrane fragments could also contribute to the capacity to proliferate, because lipids are highly energetic claiming components to establish. Trogocytosis might have appeared first in very primitive organisms to feed off other cells. Most of the biological functions identified for trogocytosis have been reported for lymphocytes and dendritic cells. Major findings along these lines are : - cytotoxic T lymphocytes having captured antigenic peptide-MHC complexes can be killed by CTL specific for this antigen (a process termed « fratricide ») - helper T lymphocyte having captured antigenic peptide-MHC complexes are involved in a negative regulatory feed-back loop leading to their inactivation - dendritic cells stripped of antigenic peptide-MHC complexes by T cells through trogocytosis contribute to affinity maturation of T cell response by seleting high affinity T cell - down-modulation of costimulatory molecules on dendritic cells mediated by T cells leads to regulation of T cell response - transfer of antigen between dendritic cells by trogocytosis favours reactivation of memory T cells at the expenses of naive T cells - transfer of antigen between dendritic cells by trogocytosis contributes to allograft rejection