C1q interactions with cell surface receptors.

The defense mechanisms initiated by the human body against foreign entities such as invading pathogenic bacteria and viruses involve intricate sequences of interactions between cells and macromolecules of the immune system. The complement system is a multienzymatic cascade which upon activation by either of two distinct mechanisms leads to the assembly of a common membranolytic complex of proteins, as well as the generation of protein fragments which mediate inflammation and enhance phagocytosis. It has now been clearly established that C1q, the initial component of the classical complement pathway, interacts in a specific manner with several immunologically important cell types, including B cells, monocytes, macrophages and polymorphonuclear leukocytes. Thus it has an uncommon potential for participating in a cellular-humoral immune network. Furthermore, since it binds both antibody-antigen complexes and other non-antibody containing activators of the classical complement pathway, C1q could provide a very efficient, direct means of modulating the immune response especially during early stages of disease when little or no antibody is present. In vitro, C1q has been shown to be capable of stimulating a number of potentially useful immune cell functions including the enhancement of phagocytosis, stimulation of oxygen radical generation and stimulation of immunoglobulin secretion. In addition, individuals which are genetically C1q-deficient develop immune-complex related disease (primarily lupus-like) and/or have severe bouts with infection. Thus, while the structure and mode of action of the cell surface C1q receptor(s) are currently unclear, it is clear that C1q has multiple significant effects on cellular immune function.