Immunodominance of H60 is caused by an abnormally high precursor T cell pool directed against its unique minor histocompatibility antigen peptide.
Document Type
Article
Publication Date
2002
Keywords
Antigen-Presentation, Flow-Cytometry, Human, Immunodominant-Epitopes, Ligands, Mice, Minor-Histocompatibility-Antigens, Minor-Histocompatibility-Loci, Organ-Transplantation, Receptors-Immunologic, SUPPORT-U-S-GOVT-P-H-S, Transplantation-Immunology
First Page
593
Last Page
603
JAX Source
Immunity 2002 Nov; 17(5):593-603.
Grant
AI28802/AI/NIAID, HL54977/HL/NHLBI, HL65479/HL/NHLBI
Abstract
The H60 minor histocompatibility (H) antigen peptide is derived from a glycoprotein that serves as a ligand for the stimulatory NKG2D receptor. We show that this peptide is remarkably immunodominant in that it competes effectively with MHC alloantigens, is efficiently crosspresented by host antigen-presenting cells (APCs), and readily elicits naive CD8 T cell responses in vitro. H60 immunodominance is neither a consequence of NKG2D engagement nor competition among minor H antigens on APCs. Instead, H60 immunodominance is a consequence of an abnormally high naive precursor frequency of H60 peptide reactive CD8 T cells. Understanding why the H60 peptide is so immunogenic has important implications in tissue transplantation and vaccine design.
Recommended Citation
Choi EY,
Christianson GJ,
Yoshimura Y,
Sproule TJ,
Jung N,
Joyce S,
Roopenian DC.
Immunodominance of H60 is caused by an abnormally high precursor T cell pool directed against its unique minor histocompatibility antigen peptide. Immunity 2002 Nov; 17(5):593-603.