Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1997-5-22
pubmed:abstractText
Peptides derived from endogenous and exogenous antigens compete for binding and presentation via class II molecules. Studies with mutant B cell lines defective in exogenous antigen presentation suggest that HLA-DM molecules facilitate the interaction of foreign peptides and class II molecules. In contrast, presentation of self antigens is not strictly dependent upon HLA-DM, as demonstrated by the ability of these mutant cells to activate T cells specific for endogenous antigens. Two distinct classes of DM-negative cells, T2 cells generated by in vitro mutagenesis and lines derived from bare lymphocyte syndrome (BLS) patients, were able to present epitopes derived from self proteins. Transfection of DM genes into the mutant cells enhanced the presentation of some, but not all, endogenous antigens, suggesting that formation of select endogenous peptide/class II complexes is not dependent upon DM. The efficiency of endogenous antigen presentation in the absence of DM was also dependent on the mutant antigen-presenting cell studied, as the TxB hybrid T2 presented greater amounts of self peptides compared to cells from BLS patients. Thus, additional genes, aside from DM, may regulate the pathway for endogenous antigen presentation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1014-21
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Presentation of abundant endogenous class II DR-restricted antigens by DM-negative B cell lines.
pubmed:affiliation
Department of Immunology, University of Washington School of Medicine, Seattle 98195, USA. skovats@u.washington.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't