Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1989-2-21
pubmed:abstractText
Cytotoxic T lymphocytes (CTLs) recognize antigens in the context of major histocompatibility complex (MHC) class I gene products. The T-cell receptor (TCR) that mediates this MHC-restricted antigen recognition recognizes short peptide fragments rather than the intact antigen. Presentation of peptides to the TCR may thus be a major function of the MHC. An intriguing question emerging from this model is whether peptide presentation also applies to foreign MHC antigens and which of the available MHC molecules can present preferentially the peptides of the foreign MHC molecule. Allo- and xenoreactive CTLs might either recognize native MHC class I molecules or peptides presented by self MHC or by the foreign class I MHC itself. The finding that synthetic peptides corresponding to MHC class I regions are recognized by allo- and xenoreactive CTLs suggests that recognition of foreign MHC by CTLs might involve degraded fragments presented by syngeneic class I molecules. We used MHC transgenic mice as a tool to study these questions. The CTL responses against human (HLA) antigen B27 were analyzed by using HLA-B27 transgenic mice with various H-2 haplotypes. We report here that mouse xeno-MHC-specific (anti-B27) CTLs are perfectly able to kill human and mouse cells expressing the appropriate xenoantigen and that in primary and secondary responses to xeno-MHC, the mouse T-cell repertoire does not use self-H-2 as a restriction element. Absence of H-2 restriction was confirmed by the lack (less than 1/10(6] of H-2-restricted HLA-specific CTL precursors. Therefore, H-2-restricted recognition of xeno-MHC antigens cannot be generalized as part of a classical MHC class I-specific response. These results indicate that xenoreactive CTLs usually recognize intact MHC molecules or MHC peptides preferentially presented by their native MHC molecule. We suggest the latter possibility.
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-141046, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-2440691, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-2443855, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-2821399, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-2834454, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-300293, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-300484, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3025085, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3082973, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3086429, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3258650, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3301331, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3309677, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3491326, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3491988, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3494999, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3501071, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-3522244, http://linkedlifedata.com/resource/pubmed/commentcorrection/2783490-6609988
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:volume
86
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
617-20
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
Recognition of xeno-(HLA, SLA) major histocompatibility complex antigens by mouse cytotoxic T cells is not H-2 restricted: a study with transgenic mice.
pubmed:affiliation
Central Laboratory, The Netherlands Red Cross Blood Transfusion Service, University of Amsterdam.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't