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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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The H4b minor histocompatibility antigen is caused by a combination of genetically determined and posttranslational modifications.

Minor histocompatibility (H) Ag disparities result in graft-vs-host disease and chronic solid allograft rejection in MHC-identical donor-recipient combinations. Minor H Ags are self protein-derived peptides presented by MHC class I molecules. Most arise as a consequence of allelic variation in the bound peptide (p) that results in TCR recognizing the p/ MHC as foreign. We used a combinational peptide screening approach to identify the immune dominant H2K(b)-restricted epitope defining the mouse H4(b) minor H Ag. H4(b) is a consequence of a P3 threonine to isoleucine change in the MHC- bound peptide derived from epithelial membrane protein-3. This allelic variation also leads to phosphorylation of the H4(b) but not the H4(a) epitope. Further, ex vivo CD8(+) T lymphocytes bind phosphorylated Ag tetramers with high efficiency. Although we document the above process in the minor H Ag system, posttranslational modifications made possible by subtle amino acid changes could also contribute to immunogenicity and immune dominance in tumor immunotherapeutic settings.[1]

References

  1. The H4b minor histocompatibility antigen is caused by a combination of genetically determined and posttranslational modifications. Yadav, R., Yoshimura, Y., Boesteanu, A., Christianson, G.J., Ajayi, W.U., Shashidharamurthy, R., Stanic, A.K., Roopenian, D.C., Joyce, S. J. Immunol. (2003) [Pubmed]
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