{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2023,10,8]],"date-time":"2023-10-08T06:42:05Z","timestamp":1696747325872},"reference-count":29,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2005,12,5]],"date-time":"2005-12-05T00:00:00Z","timestamp":1133740800000},"content-version":"vor","delay-in-days":12301,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[1972,4]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>During incubation of zymosan with human or guinea pig serum, a complex is fixed on the polysaccharide which, after washing, releases anaphylatoxin from C5 when incubated with an anaphylatoxinogen preparation from rat serum containing C3 and C5. In order to form this complex, properdin and an unknown serum factor (UF), as well as high serum concentrations (not less than 1:4), are needed. No anti\u2010zymosan antibodies need be added. The complexes consume little C2 from serum and are active in anaphylatoxin (AT) liberation in small amounts (3 mg zymosan complex\/ml substrate). After spontaneous decay of the AT\u2010forming activity, regeneration is affected by addition of UF, not by C2.<\/jats:p><jats:p>Zymosan\u2010R3<jats:sub>g.p.<\/jats:sub>, <jats:italic>i.e.<\/jats:italic> guinea pig serum lacking properdin and UF because of pretreatment with zymosan, does not coat fresh zymosan with an active AT\u2010liberating complex, although it contains C1, C4, and C2. However, it does coat zymosan to which large amounts of rabbit anti\u2010zymosan antibodies have already been fixed. The resulting complement complex ZAC 142 forms at serum (R3) dilutions of 1:10 also. It effectively releases AT from substrate only when present in high amounts (20 mg\/ml substrate); it largely consumes C2 from serum, and it is less active as an AT\u2010forming system than the zymosan properdin complex. Thus, two different AT\u2010forming systems can be activated by and fixed to zymosan, both derived from serum factors.<\/jats:p><jats:p>No evidence for activation or fixation of the properdin system by sheep red cells was found. Red cells appear to release AT only <jats:italic>via<\/jats:italic> the complex of early complement factors. It is probably the special polysaccharide surface which enables zymosan and possibly other (lipo)polysaccharides to fix the properdin system.<\/jats:p>","DOI":"10.1002\/eji.1830020216","type":"journal-article","created":{"date-parts":[[2007,2,27]],"date-time":"2007-02-27T21:36:49Z","timestamp":1172612209000},"page":"180-186","source":"Crossref","is-referenced-by-count":1,"title":["Anaphylatoxin formation by contact activation of plasma III. 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