Linked Life Data

7911423

Source:http://linkedlifedata.com/resource/pubmed/id/7911423

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1994-7-8
pubmed:abstractText
Sequence polymorphism has been reported for virtually all malaria antigens and, in the case of the circumsporozoite (CS) protein, this variation is in the form of point mutations concentrated primarily in several regions recognized by T cells. The factors responsible for the variation are unknown. We studied the T cell responses to all known variants in malaria-exposed Thais. Memory CD4+ T cells responded to variants of a polymorphic immunodominant region (denoted Th2R), and CD4+ T cell clones specific for one Thai Th2R variant were generated. There was minimal cross-reactivity to any of the naturally occurring variants, including the other Thai variant, and competition studies performed with the clones using analog peptides demonstrated that all the substitutions of the polymorphic residues modulate either the binding of the peptide to major histocompatibility complex (MHC) molecules or the recognition by the T cell receptor of the peptide-MHC complex. Our data suggest that CD4+ T cells may be able to select parasites expressing variant sequences and have implications for development of a CS-based vaccine.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
24
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1418-25
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Natural amino acid polymorphisms of the circumsporozoite protein of Plasmodium falciparum abrogate specific human CD4+ T cell responsiveness.
pubmed:affiliation
Molecular Immunology Laboratory, Queensland Institute of Medical Research, Brisbane, QLD, Australia.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't