Cell-mediated immunity: The role of bacterial protein secretion

Most eukaryotic cells express major histocompatibility complex (MHC) class I molecules on their surface. These immune molecules present peptide fragments derived from the breakdown of proteins in the cell to CD8+ cytotoxic T lymphocytes (CTLs), which recognize the peptide–MHC complexes via T-cell receptors (TCRs) expressed on their surface [1]. In uninfected cells, the peptides that are bound within the cleft of MHC class I molecules are derived from self-encoded proteins and do not activate the CTLs. During infection, however, some of the peptides that are presented on the cell surface by MHC class I molecules derive from intracellular pathogens. These peptides are recognized by CTLs as being foreign, thereby inducing activation, proliferation and expansion of these cells into an effector population that can directly combat infection and also give rise to memory CTLs that rapidly curtail repeat infections with the same pathogen. A critical aspect of this process is that CTLs only recognize foreign peptides that are presented by self-MHC class I molecules, hence the concept of MHC restriction [2].