TY - JOUR
T1 - Alloreactive CD8+ T Cells Can Recognize Unusual, Rare, and Unique Processed Peptide/MHC Complexes
AU - Malarkannan, Subramaniam
AU - Gonzalez, Federico
AU - Nguyen, Vu
AU - Adair, Gerald
AU - Shastri, Nilabh
PY - 1996/11/15
Y1 - 1996/11/15
N2 - The identity and abundance of self-peptide/MHC class I complexes that serve as ligands for alloreactive T cells remain largely unknown. Using the Kb-restricted, alloreactive T cells as a probe, the Ag precursor gene, adenosine phosphoribosyl transferase (APRT), was isolated by expression cloning. Its naturally processed product was identified as the SLVELTSL (SEL8) octapeptide. The SEL8 peptide shared five residues with the previously identified SVVEFSSL (JAL8) peptide that stimulated the same T cell, but lacked the critical phenylalanine/tyrosine residue at the primary p5 anchor position. Despite the absence of this key conserved anchor residue, SEL8 was bound tightly by Kb MHC and yet was expressed at less than 10 copies/cell. Mutations in the donor APRT gene in the APC caused a concomitant loss in the ability of APCs to stimulate T cells. The results confirm that the display of peptide/MHC complexes in cells exceeds the predictions based upon consensus motifs, and that CD8+ alloreactive and conventional Ag-specific T cells are indistinguishable in their ability to recognize unique and rare peptide/MHC class I complexes.
AB - The identity and abundance of self-peptide/MHC class I complexes that serve as ligands for alloreactive T cells remain largely unknown. Using the Kb-restricted, alloreactive T cells as a probe, the Ag precursor gene, adenosine phosphoribosyl transferase (APRT), was isolated by expression cloning. Its naturally processed product was identified as the SLVELTSL (SEL8) octapeptide. The SEL8 peptide shared five residues with the previously identified SVVEFSSL (JAL8) peptide that stimulated the same T cell, but lacked the critical phenylalanine/tyrosine residue at the primary p5 anchor position. Despite the absence of this key conserved anchor residue, SEL8 was bound tightly by Kb MHC and yet was expressed at less than 10 copies/cell. Mutations in the donor APRT gene in the APC caused a concomitant loss in the ability of APCs to stimulate T cells. The results confirm that the display of peptide/MHC complexes in cells exceeds the predictions based upon consensus motifs, and that CD8+ alloreactive and conventional Ag-specific T cells are indistinguishable in their ability to recognize unique and rare peptide/MHC class I complexes.
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M3 - Article
C2 - 8906823
AN - SCOPUS:0030588548
SN - 0022-1767
VL - 157
SP - 4464
EP - 4473
JO - Journal of Immunology
JF - Journal of Immunology
IS - 10
ER -