Publication | Open Access
Cell stress-regulated human major histocompatibility complex class I gene expressed in gastrointestinal epithelium.
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1996
Year
HistocompatibilityMhc ClassImmunologyImmune RegulationPathologyAntigen ProcessingImmunotherapyCellular PhysiologyImmunogeneticsTranscriptional RegulationCell RegulationCell SignalingGastrointestinal EpitheliumAutoimmune DiseaseAutoimmunityHsp70 GenesGene ExpressionCell BiologyCell Surface GlycoproteinMucosal ImmunologyGene RegulationMedicine
Conventional MHC class I genes encode peptide‑presenting molecules regulated by interferon‑γ, whereas the divergent genes MICA and MICB are controlled by heat‑shock promoter elements similar to HSP70. MICA encodes a β2‑microglobulin‑independent, peptide‑ligand‑stable glycoprotein expressed almost exclusively in gastrointestinal epithelium, suggesting it signals cell stress and may engage a subset of gut mucosal T cells.
Conventional major histocompatibility complex (MHC) class I genes encode molecules that present intracellular peptide antigens to T cells. They are ubiquitously expressed and regulated by interferon gamma. Two highly divergent human MHC class I genes, MICA and MICB, are regulated by promoter heat shock elements similar to those of HSP70 genes. MICA encodes a cell surface glycoprotein, which is not associated with beta 2-microglobulin, is conformationally stable independent of conventional class I peptide ligands, and almost exclusively expressed in gastrointestinal epithelium. Thus, this MHC class I molecule may function as an indicator of cell stress and may be recognized by a subset of gut mucosal T cells in an unusual interaction.
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