A new mode of Cytotoxic T lymphocyte induction secondary to alteration of the peptide/major histocompatibility complex class I repertoire by antigen processing defects

Abstract

The cell surface repertoire of peptide/major histocompatibility complex (MHC) class I (pMHCI) provides potential ligands for circulating CD8 + cytotoxic T lymphocytes (CTLs). Because the action of antigen-processing machineries inside cells are necessary for optimizing pMHCI formation, it has been believed that antigen- processing defect (APD) attenuates any CTL responses. However, recent evidences demonstrate that the cells with APD often present a unique pMHCI repertoire harboring immunogenic peptides that are never displayed on normal cells. Here we focus on the absence of endoplasmic reticulum (ER)-resident editors ERAAP or tapasin and discuss a new mode of CTL induction secondary to it.