Abstract
The complement system is a major humoral component of immunity and is essential for the fast elimination of pathogens invading the body. In addition to its indispensable role in innate immunity, the complement system is also involved in pathogen clearance during the effector phase of adaptive immunity. The fastest way of killing the invader is lysis by the membrane attack complex, which is formed by the terminal components of the complement cascade. Not all pathogens are lysed however and, if opsonized by a variety of molecules, they undergo phagocytosis and disposal inside immune cells. The most important complement-derived opsonins are C1q, the first component of the classical pathway, MBL, the initiator of the lectin pathway and C3-derived activation fragments, including C3b, iC3b and C3d, which all serve as ligands for their corresponding receptors. In this review, we discuss how complement receptors are utilized by various immune cells to tackle invading microbes, or by pathogens to evade host response.
Highlights
Szilvia Lukacsi1, Bernadett Macsik-Valent1, Zsuzsa Nagy-Balo2, Kristof G
As surface-bound factor H can enhance the antifungal activity via binding to CR3 and CR4, C. albicans avoid phagocytosis by releasing the secreted aspartic protease 2 (Sap2) to cleave both FH and the complement receptors CR3 and CR4 on macrophages [75]
Hepatitis C virus (HCV) core protein engagement of gC1qR on dendritic cells promoted the production of Th2 cytokines such as IL-4 by cocultured CD4+ T cells. These results suggest that the engagement of gC1qR on dendritic cells by HCV limits the induction of a Th1 response [131]
Summary
Szilvia Lukacsi1 , Bernadett Macsik-Valent1, Zsuzsa Nagy-Balo2, Kristof G. The immune complex formation of virus envelope protein-specific antibodies and HIV-1 leads to opsonization and binding to CR1 on K562 leukaemia-derived cell line [14]. To monocytes and macrophages, opsonization of HIV-1 with complement leads to earlier and enhanced infection of CD4-expressing human T-cell lines in a CR1- or CR2-dependent manner, as blocking either of these receptors diminished the positive effect of complement [19].
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