Four synthetic saccharides (mono-, di-, tri-, tetra-) linked to the carrier 8-methoxycarbonyloctanol were used in the presence or absence of a polysaccharide (PS) purified from ant venom to study the activation of C1 and the consumption of C4 in normal serum. The carrier was essential for the recorded activities of the saccharides. The αD mannose-O-carrier did not cause C1 activation and C4 consumption by itself, but it enhanced these activities when combined with the venom PS. The αL fuc(1 → 4)βD glc-NAc-O-carrier caused C1 activation but no C4 consumption by itself at a high concentration (1.4 mg/ml), and enhanced C1 activation and C4 consumption in combination with the venom PS. The βD gal(1 → 3)αL fuc(1 → 4)βD glc-NAc-O-carrier caused both C1 activation and C4 consumption in normal human serum by itself. The αL fuc(1 → 2)βD gal[αL fuc(1 → 4)]βD glc NAc-O-carrier neither caused C1 activation and C4 consumption by itself, nor did it enhance these activities when combined with the venom PS. Neither EAC1(hu) nor EAC1(hu) bound 3H-PS or 3H-βD gal(1 → 3)αL fuc(1 → 4)βD glc-NAc-O-carrier. Also, the precursor human C1 on EA (EAC1) was not activated by the venom PS. Thus, the overall evidence shows that human precursor C1 is activated by these carbohydrates solely by an interaction with C1q subunit of macromolecular C1.
|Original language||English (US)|
|Number of pages||5|
|Journal||Journal of Immunology|
|State||Published - Jan 1 1981|
ASJC Scopus subject areas
- Immunology and Allergy