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Abstract
Our understanding of the biology of the complement system has undergone a drastic
metamorphosis since its original discovery. This system, which was traditionally primarily
described as a "complement" to humoral immunity, is now perceived as a central constituent
of innate immunity, defending the host against pathogens, coordinating various events
during inflammation, and bridging innate and adaptive immune responses. Complement
is an assembly of proteins found in the blood and body fluids and on cell surfaces.
Soluble complement components form the proteolytic cascade, whose activation leads
to the generation of complement effectors that target various cells involved in the
immune response. Membrane-bound receptors and regulators transmit signals from complement
effectors to target cells and limit complement activation to the surfaces of pathogens
and damaged or activated host cells. The multiple interconnections among complement
proteins, immune cells, and mediators provide an excellent mechanism to protect the
organism against infections and support the repair of damaged tissues. However, disturbances
in this "defense machinery" contribute to the pathogenesis of various diseases. The
role of complement in various inflammatory disorders is multifaceted; for example,
the activation of complement can significantly contribute to inflammation-mediated
tissue damage, whereas inherited or acquired complement deficiencies highly favor
the development of autoimmunity.