title: [Role of the classical and alternative complement pathways in chemotaxis of human C2 deficiency (author's transl)].
abstract: The roles of the classical and alternative complement pathways in the formation of chemotactic factors were comparatively evaluated in a normal serum and a serum from a child with congenital C2 deficiency. Neutrophil chemotactic index was determined by a direct microscopic observation using serum activated by an immune complex for the classical pathway, and by zymosan A or liposaccharide of Salmonella enteritidis for the alternative pathway. Chemotactic activity was observed only when the C2-deficient serum was activited by the alternative pathway in the presence of zymosan A. But, in comparison to normal serum, the chemotactic activity of C2-deficient serum was impaired by dilution or short incubation time. Addition of purified C2 resulted in the normalisation of chemotactic activity induced by activation of classical and alternative pathways. These results suggest that integrity of the classical pathway of the complement is necessary for the optimal formation of the chemotactic mediators induced by the alternative complement pathway. The implications of the alternative complement pathway alteration with regard to susceptibility to bacterial infections, are discussed.
mesh_terms: D000936:Antigen-Antibody Complex; D001424:Bacterial Infections / Q000276:immunology; D002630:Chemotactic Factors / Q000096:biosynthesis; D002675:Child, Preschool; D003167:Complement Activation; D003175:Complement C2 / Q000172:deficiency*; D003170:Complement Pathway, Alternative; D003171:Complement Pathway, Classical; D006801:Humans; D007700:Kinetics; D008070:Lipopolysaccharides / Q000494:pharmacology; D015054:Zymosan / Q000494:pharmacology
chemical_list: D000936:Antigen-Antibody Complex; D002630:Chemotactic Factors; D003175:Complement C2; D008070:Lipopolysaccharides; D015054:Zymosan
vernacular_title: Formation de facteurs chimiotactiques par activation des voies classique ou alterne du complément d'un sérum déficient en C2.