Linked Life Data

6854021

Source:http://linkedlifedata.com/resource/pubmed/id/6854021

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1983-7-8
pubmed:abstractText
Circulating IgA which does not bind the first component of complement (C) and does not activate the classical C pathway, blocks the initiation of C-mediated immune effector mechanisms. In at least two clinical situations, epidemic meningococcal disease and severe hepatic dysfunction, IgA blockade of one such mechanism, immune lysis, results in susceptibility to hematogenous bacterial dissemination. The presence of strain-specific IgM, but not IgG, in the sera of susceptibles at the time of dissemination suggested that IgA blockade of IgM-initiated lysis involves a separate mechanism more sensitive to quantitative changes than that involved in IgA blockade of IgG-initiated lysis. We report here that whereas IgA blockade of IgG-initiated immune lysis is a competitive function of the ratio of IgA to IgG, the blocking of IgM-initiated lysis is a noncompetitive function of the ratio of IgA to target cells, independent of the concentration of IgM. In the presence of sufficient IgA to saturate binding sites, IgM is an impotent bystander unable to compete for sites or initiate lysis. Therefore, C-mediated effector mechanisms are more sensitive to quantitative changes in circulating IgA and target cells (binding sites) in the absence of IgG than in its presence. Neither mechanism appears related to binding kinetics.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
130
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2882-5
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
IgA blocks IgM and IgG-initiated immune lysis by separate molecular mechanisms.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.