Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1992-2-13
pubmed:abstractText
Anti-idiotypic antibodies (Ab2) binding to the antigen-combining site of other antibodies may functionally and even structurally mimic antigen. Ab2 to antibodies directed against the lymphocyte CD4 receptor for human immunodeficiency virus type 1 (HIV-1) may mimic the receptor and therefore inhibit viral infectivity. We have produced Ab2 against monoclonal anti-CD4 receptor antibodies (Ab1). The Ab1 strongly inhibit HIV-1 binding to the receptor. Six monoclonal rat Ab2 and two polyclonal rabbit Ab2 were produced against the Ab1 MT151 and nine monoclonal Ab2 against the Ab1 OKT4A. These Ab2 bound only to Ab1 and not to a panel of nine unrelated murine monoclonal antibodies (MAbs). The Ab2 completely inhibited the binding of the homologous Ab1 to CD4-positive target cells, and recombinant soluble CD4 inhibited binding of Ab2 to Ab1. Thus, the Ab2 seemed to mimic the Ab1-binding site of the CD4 receptor, although the results of inhibition assays did not exclude steric hindrance of antibody-combining sites. However, none of the 17 Ab2 bound to gp120 of HIV-1 envelope or inhibited syncytia formation between cells infected and uninfected with HIV-1. These results suggest that the Ab2 do not mimic the HIV-1 binding site of the CD4 receptor. They further suggest that the Ab1 may not bind within the virus-binding site of the CD4 receptor.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0882-8245
pubmed:author
pubmed:issnType
Print
pubmed:volume
4
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
83-90
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Anti-idiotypic antibodies against anti-CD4 antibodies MT151 and OKT4A.
pubmed:affiliation
Wistar Institute, Philadelphia, Pennsylvania.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.