With the antigen classical pathway of complement system pdf in opsonins, binding to immune cells is greatly enhanced. Opsonization also mediates phagocytosis via signal cascades from cell surface receptors.
Opsonins aid the immune system in a number of ways. When opsonins bind to their targets they boost the kinetics of phagocytosis by favoring interaction between the opsonin and cell surface receptors on immune cells. This overrides the negative charges from cell membranes. Different opsonins perform different functions. B cells in response to antigen exposure.
IgM ineffective in assisting phagocytosis alone. C3b, C4b, and C1q are important complement molecules that serve as opsonins. Antibodies can also activate complement via the classical pathway, resulting in deposition of C3b and C4b onto the antigen surface. After C3b has bound to the surface of an antigen, it can be recognized by phagocyte receptors that signal for phagocytosis. These molecules coat the microbes as opsonins and enhance neutrophil reactivity against them through a number of mechanisms.
Apoptosis is related to low tissue inflammation. A number of opsonins play a role in marking apoptotic cells for phagocytosis without a pro-inflammatory response. When bound to the appropriate ligand these molecules interact with phagocyte receptors, enhancing phagocytosis of the marked cell. It can also indirectly bind to apoptotic cells via intermediates like IgM autoantibodies, MBL, and pentraxins.
C1q is an important contributor to the clearance of apoptotic cells and debris. This process usually occurs in late apoptotic cells. Opsonization of apoptotic cells occurs by different mechanisms in a tissue-dependent pattern. For example, while C1q is necessary for proper apoptotic cell clearance in the peritoneal cavity, it is not important in the lungs where SP-D plays an important role. As part of the late stage adaptive immune response, pathogens and other particles are marked by IgG antibodies.
IgG and IgM immune complexes activating the classical complement pathway and marking the antigen with C3b. C3b can spontaneously bind to pathogen surfaces through the alternative complement pathway. Furthermore, pentraxins can directly bind to C1q from the C1 complex. SP-A opsonizes a number of bacterial and viral pathogens for clearance by lung alveolar macrophages.