TY - JOUR
T1 - Different MHC class I alleles compete for presentation of overlapping viral epitopes
AU - Tussey, Lynda G.
AU - Rowland-Jones, Sarah
AU - Zheng, Timothy S.
AU - Androlewicz, Matthew J.
AU - Cresswell, Peter
AU - Frelinger, Jeffrey A.
AU - McMichael, Andrew J.
N1 - Funding Information:
The authors thank V. Cerundolo and C. Ohlen for helpful discussions of the data. We thank V. Cerundolo for help with the HW CTL. This work was supported by the Medical Research Council and National Institutes of Health grants Al 26266 and Al 29324. L. G. T. is supported by Wellcome Trust Hitching!+Elion Foundation Fellowship 5F32 Al06344-02.
PY - 1995/7
Y1 - 1995/7
N2 - We previously identified an HLA-B8+ donor, NW, whose lymphoblestoid cells failed to present a B8-restricted epitope from the influenza A nucleoprotein following viral infection, although added peptide could still be presented. The failure to present through HLA-B8 following viral infection appears to be specific for the NP epitope. Here, we report that donor NW makes an HLA-132702-restricted influenza-specific CTL response to an epitops in the nucleoprotein that overlaps the 138-restricted epitope by 8 aa. Two mechanisms for the failure of this cell line to present the 138-restricted epitope following viral infection are investigated. One is that there is an antigen processing polymorphism specific to the NW cell line, so that there is either preferential generation or preferential transport of the B27702 epitope. The other is that 138 and 132702 compete for a common peptide fragment in the ER and this leads to suboptimal loading of HLA-138.
AB - We previously identified an HLA-B8+ donor, NW, whose lymphoblestoid cells failed to present a B8-restricted epitope from the influenza A nucleoprotein following viral infection, although added peptide could still be presented. The failure to present through HLA-B8 following viral infection appears to be specific for the NP epitope. Here, we report that donor NW makes an HLA-132702-restricted influenza-specific CTL response to an epitops in the nucleoprotein that overlaps the 138-restricted epitope by 8 aa. Two mechanisms for the failure of this cell line to present the 138-restricted epitope following viral infection are investigated. One is that there is an antigen processing polymorphism specific to the NW cell line, so that there is either preferential generation or preferential transport of the B27702 epitope. The other is that 138 and 132702 compete for a common peptide fragment in the ER and this leads to suboptimal loading of HLA-138.
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U2 - 10.1016/1074-7613(95)90159-0
DO - 10.1016/1074-7613(95)90159-0
M3 - Article
C2 - 7542549
AN - SCOPUS:0029135263
SN - 1074-7613
VL - 3
SP - 65
EP - 77
JO - Immunity
JF - Immunity
IS - 1
ER -