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From Proteopedia
MHC-I in complex with peptide
Structural highlights
Function[HA11_MOUSE] Involved in the presentation of foreign antigens to the immune system. [PB1F2_I34A1] Plays an important role in promoting lung pathology in both primary viral infection and secondary bacterial infection. Promotes alteration of mitochondrial morphology, dissipation of mitochondrial membrane potential, and cell death. Alternatively, inhibits the production of interferon in the infected cell at the level of host mitochondrial antiviral signaling MAVS. Its level of expression differs greatly depending on which cell type is infected, in a manner that is independent of the levels of expression of other viral proteins. Monocytic cells are more affected than epithelial cells. Seems to disable virus-infected monocytes or other host innate immune cells. May also act in trans: extracellular PB1-F2 released by infected cells could potentially inactivate hosts cell recruitment to the site of infection. During early stage of infection, may predispose the mitochondria to permeability transition through interaction with human SLC25A6/ANT3 and VDAC1. These proteins participate in the formation of the permeability transition pore complex (PTPC) responsible of the release of mitochondrial products that triggers apoptosis.[1] [B2MG_MOUSE] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. Evolutionary Conservation Check, as determined by ConSurfDB. You may read the explanation of the method and the full data available from ConSurf. Publication Abstract from PubMedTCR repertoire diversity has been convincingly shown to facilitate responsiveness of CD8+ T cell populations to mutant virus peptides, thereby safeguarding against viral escape. However, the impact of repertoire diversity on the functionality of the CD8+ T cell response to cognate peptide-MHC class I complex (pMHC) recognition remains unclear. Here, we have compared TCRbeta chain repertoires of three influenza A epitope-specific CD8+ T cell responses in C57BL/6 (B6) mice: D(b)NP(366-374), D(b)PA(224-233), and a recently described epitope derived from the +1 reading frame of the influenza viral polymerase B subunit (residues 62-70) (D(b)PB1-F2(62)). Corresponding to the relative antigenicity of the respective pMHCs, and irrespective of the location of prominent residues, the D(b)PA(224)- and D(b)PB1-F2(62)-specific repertoires were similarly diverse, whereas the D(b)NP(366) population was substantially narrower. Importantly, parallel analysis of response magnitude, cytotoxicity, TCR avidity, and cytokine production for the three epitope-specific responses revealed no obvious functional advantage conferred by increased T cell repertoire diversity. Thus, whereas a diverse repertoire may be important for recognition of epitope variants, its effect on the response to cognate pMHC recognition appears minimal. Epitope-specific TCRbeta repertoire diversity imparts no functional advantage on the CD8+ T cell response to cognate viral peptides.,La Gruta NL, Thomas PG, Webb AI, Dunstone MA, Cukalac T, Doherty PC, Purcell AW, Rossjohn J, Turner SJ Proc Natl Acad Sci U S A. 2008 Feb 12;105(6):2034-9. Epub 2008 Jan 31. PMID:18238896[2] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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Categories: Large Structures | Lk3 transgenic mice | Dunstone, M A | Gruta, N L.La | Purcell, A W | Rossjohn, J | Turner, S J | Apoptosis | Cytoplasm | Glycoprotein | Host-virus interaction | Immune response | Immune system | Immunoglobulin domain | Inner membrane | Membrane | Mhc i | Mhc-i | Mitochondrion | Nucleus | Polymorphism | Secreted | Transmembrane
