Linked Life Data

7453820

Source:http://linkedlifedata.com/resource/pubmed/id/7453820

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5794
pubmed:dateCreated
1981-3-17
pubmed:abstractText
Flaviviruses, when complexed with antibody at subneutralizing concentrations, show enhanced replication in human and simian peripheral blood leukocytes (ref. 1, and J.S.M.P. and J.S.P., unpublished observations) and in P388 D1 and other macrophage cell lines. A comparable phenomenon has been demonstrated with alphaviruses and Bunyaviruses in P388 D1 cells, (J.S.M.P. and J.S.P., unpublished observations) but cells lacking macrophage characteristics fail to show antibody-dependent enhancement (ADE) of viral replication. It has been suggested that the macrophage Fc receptor (FcR) provides an efficient route of entry of virus through the attachment of non-neutralized virus-antibody complexes and that for those viruses that escape destruction by the phagocyte, antibody results in a paradoxical increase in virus replication. West Nile virus (WNV) replication in the P388 D1 macrophage cell line provides a reproducible model system for studying ADE of viral replication. Mouse macrophages have two FcRs-FcRI, which is trypsin-sensitive and binds IgG2a, and FcRII, which is trypsin-resistant and binds IgG2b and IgG1 complexes. The FcR has been purified using rat anti-mouse FcR monoclonal antibody which blocks FcRII. We show here that anti-FcRIgG and its Fab fragment block ADE of virus replication by anti-WNV monoclonal antibodies.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
289
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
189-91
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1981
pubmed:articleTitle
Monoclonal anti-Fc receptor IgG blocks antibody enhancement of viral replication in macrophages.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't