Abstract:C1q, a component of the classical complement pathway, is required for clearance of apoptotic cells. C1q also regulates activation of innate immune cells through engagement of C1q receptors present on the immune cell surface. C1q deficiency is highly associated with the development of systemic lupus erythematosus (SLE). High Mobility Group Box 1 (HMGB1), a pro-inflammatory mediator, is secreted by inflammatory cells and passively released from necrotic cells. HMGB1 interacts with TLR4 and receptor for advanced … Show more
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