Uncoupling complement C1s activation from C1q binding in apoptotic cell phagocytosis and immunosuppressive capacity.

摘要: Complement activation contributes to inflammation in many diseases, yet it also supports physiologic apoptotic cells (AC) clearance and its downstream immunosuppressive effects. The roles of individual complement components AC phagocytosis have been difficult dissect with artificially depleted sera. Using human vitro systems the novel antibody C1s inhibitor TNT003, we uncoupled role enzymatic classical pathway from opsonizing C1q mediating a) early late AC, b) capacity AC. We found that inhibition had a small impact on leaving their properties entirely unaffected, while mainly inhibiting apoptotic/secondary necrotic cells. Our data suggest may represent valuable therapeutic strategy control without causing significant accumulation diseases defects phagocytosis.