Molecular regulation of immune-complex induced neutrophil functions
mardi 18 février 2020
Amphithéâtre Fisher, Local T-054, Site CHUL
10 h 00
Conférence présentée par Dre Sonja Vermeren, University of Edinburgh, The Queen's Medical Research Institute, Centre for Inflammation Research, U.K.
Résumé de la conférence :
Neutrophils are the most abundant circulating leukocytes in man. These short-lived innate immune cells are key players in the inflammatory response and provide a cellular first line of defense against infections.
Upon activation neutrophils leave the blood stream to travel to sites of infection or injury. There they kill pathogens, employing reactive oxygen species in combination with powerful proteases and other cytotoxic compounds. Inappropriately activated neutrophils can inflict important host injury. Immune complexes, drivers of autoimmune diseases such as rheumatoid arthritis, potently activate neutrophils to induce a range of effector functions. We recently showed that in addition to inducing a range of proinflammatory neutrophil functions, insoluble immune complexes also promote neutrophil apoptosis. Our latest observations illustrate that neutrophils internalise and clear immune complexes, as well as undergoing apoptosis. Neutrophil apoptosis is regarded as a pro-resolution event, where apoptotic neutrophils display eat-me signals that target them for efferocytosis by pro-resolution macrophages. Given the prominent role of immune complexes in driving autoimmune disease, the observation that neutrophils clear these complexes, while also undergoing apoptosis suggests that immune complex-induced neutrophil apoptosis are protective mechanisms aimed at avoiding the inappropriate activation of neutrophils, and thereby excessive host damage.