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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
3
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pubmed:dateCreated |
1982-8-14
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pubmed:abstractText |
This study has examined the mechanisms involved in complement-mediated inhibition of immune precipitation using radiolabelled BSA and rabbit anti-BSA. Purified proenzyme C1 was capable of maintaining the complexes in soluble form during the first few minutes of reaction whereas immune precipitation was immediate in the presence of purified C1q or C1 + EDTA (ethylenediamine tetra-acetate). In C1q deficient serum, initial immune aggregation was followed by partial solubilization of the formed precipitate similar to that obtained with normal human serum in the presence of Mg EGTA. In C2 deficient serum precipitation occurred at a slow rate. Repletion of the deficient component (C1q or C2 respectively) restored fully inhibition of precipitation. These experiments establish a critical role for the classical pathway, in this phenomenon. By contrast the role of the alternative pathway in maintaining complexes in solution was less important; only partial and delayed precipitation occurred in sera depleted of factor D (RD) or factor B (RB). B and D restored normal complement activity to depleted sera. No precipitation was detected in a reagent depleted of properdin (RP). The mechanisms of inhibition of precipitation are therefore distinct from those responsible for solubilization of an immune precipitate, which is largely dependent on the alternative pathway.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-1054824,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-118112,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-1249522,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-13838615,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-4098878,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-4100767,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-441683,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-458153,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-521056,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-6158260,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-6170880,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-6445507,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-670397,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-6781802,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-700771,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-79721,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-830792,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-944196,
http://linkedlifedata.com/resource/pubmed/commentcorrection/6979442-985398
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0009-9104
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
47
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
555-62
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:6979442-Animals,
pubmed-meshheading:6979442-Antigen-Antibody Complex,
pubmed-meshheading:6979442-Complement Activating Enzymes,
pubmed-meshheading:6979442-Complement Activation,
pubmed-meshheading:6979442-Complement C1,
pubmed-meshheading:6979442-Complement C1q,
pubmed-meshheading:6979442-Complement C2,
pubmed-meshheading:6979442-Complement Pathway, Alternative,
pubmed-meshheading:6979442-Complement Pathway, Classical,
pubmed-meshheading:6979442-Complement System Proteins,
pubmed-meshheading:6979442-Humans,
pubmed-meshheading:6979442-Rabbits,
pubmed-meshheading:6979442-Solubility
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pubmed:year |
1982
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pubmed:articleTitle |
Complement-mediated inhibition of immune precipitation. I. Role of the classical and alternative pathways.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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