IT has been well appreciated for many years that the serum complement system, through the concerted action of all its components, is a prime mediator of cytotoxic injury to antibody-sensitized cells. In the last several years, other functions that contribute to the inflammatory process have been attributed to reaction products of the activation of the terminal portion of the system (C3, C5 ... C9). For example, peptides derived from C3 and C5 are potent mediators of histamine release, smooth-muscle contraction, and enhancement of vascular permeability. Other examples of the phlogistic consequences of complement activation reside in the enhanced susceptibility to . . .
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Lepow et al. (1972) studied this question.
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