4l8c: Difference between revisions
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==Crystal structure of the H2Db in complex with the NP-N3D peptide== | |||
<StructureSection load='4l8c' size='340' side='right' caption='[[4l8c]], [[Resolution|resolution]] 2.80Å' scene=''> | |||
== Structural highlights == | |||
<table><tr><td colspan='2'>[[4l8c]] is a 12 chain structure with sequence from [http://en.wikipedia.org/wiki/Lk3_transgenic_mice Lk3 transgenic mice]. Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=4L8C OCA]. For a <b>guided tour on the structure components</b> use [http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4L8C FirstGlance]. <br> | |||
</td></tr><tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat"><scene name='pdbligand=SO4:SULFATE+ION'>SO4</scene></td></tr> | |||
<tr id='related'><td class="sblockLbl"><b>[[Related_structure|Related:]]</b></td><td class="sblockDat">[[4huu|4huu]], [[4huv|4huv]], [[4huw|4huw]], [[4hux|4hux]], [[4hv8|4hv8]], [[4l8b|4l8b]], [[4l8d|4l8d]]</td></tr> | |||
<tr id='gene'><td class="sblockLbl"><b>[[Gene|Gene:]]</b></td><td class="sblockDat">H2-D1 ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=10090 LK3 transgenic mice]), B2m ([http://www.ncbi.nlm.nih.gov/Taxonomy/Browser/wwwtax.cgi?mode=Info&srchmode=5&id=10090 LK3 transgenic mice])</td></tr> | |||
<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[http://oca.weizmann.ac.il/oca-docs/fgij/fg.htm?mol=4l8c FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=4l8c OCA], [http://www.rcsb.org/pdb/explore.do?structureId=4l8c RCSB], [http://www.ebi.ac.uk/pdbsum/4l8c PDBsum]</span></td></tr> | |||
</table> | |||
== Function == | |||
[[http://www.uniprot.org/uniprot/HA11_MOUSE HA11_MOUSE]] Involved in the presentation of foreign antigens to the immune system. [[http://www.uniprot.org/uniprot/B2MG_MOUSE B2MG_MOUSE]] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. | |||
<div style="background-color:#fffaf0;"> | |||
== Publication Abstract from PubMed == | |||
Influenza A virus-specific CD8(+) cytotoxic T lymphocytes (CTLs) provide a degree of cross-strain protection that is potentially subverted by mutation. Here we describe the sequential emergence of such variants within CTL epitopes for a persistently infected, immunocompromised infant. Further analysis in immunodeficient and wild-type mice supports the view that CTL escape variants arise frequently in influenza, accumulate with time and revert in the absence of immune pressure under MHCI-mismatched conditions. Viral fitness, the abundance of endogenous CD8(+) T cell responses and T cell receptor repertoire diversity influence the nature of these de novo mutants. Structural characterization of dominant escape variants shows how the peptide-MHCI interaction is modified to affect variant-MHCI stability. The mechanism of influenza virus escape thus looks comparable to that recognized for chronic RNA viruses like HIV and HCV, suggesting that immunocompromised patients with prolonged viral infection could have an important part in the emergence of influenza quasispecies. | |||
Acute emergence and reversion of influenza A virus quasispecies within CD8(+) T cell antigenic peptides.,Valkenburg SA, Quinones-Parra S, Gras S, Komadina N, McVernon J, Wang Z, Halim H, Iannello P, Cole C, Laurie K, Kelso A, Rossjohn J, Doherty PC, Turner SJ, Kedzierska K Nat Commun. 2013 Oct 30;4:2663. doi: 10.1038/ncomms3663. PMID:24173108<ref>PMID:24173108</ref> | |||
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.<br> | |||
</div> | |||
== | ==See Also== | ||
*[[Beta-2 microglobulin|Beta-2 microglobulin]] | |||
== References == | |||
<references/> | |||
__TOC__ | |||
</StructureSection> | |||
[[Category: Lk3 transgenic mice]] | [[Category: Lk3 transgenic mice]] | ||
[[Category: Gras, S | [[Category: Gras, S]] | ||
[[Category: Rossjohn, J | [[Category: Rossjohn, J]] | ||
[[Category: Immune system]] | [[Category: Immune system]] | ||
[[Category: Influenza]] | [[Category: Influenza]] | ||
[[Category: T cell immunity]] | [[Category: T cell immunity]] | ||
[[Category: Viral escape]] | [[Category: Viral escape]] | ||
Revision as of 18:41, 24 December 2014
Crystal structure of the H2Db in complex with the NP-N3D peptideCrystal structure of the H2Db in complex with the NP-N3D peptide
Structural highlights
Function[HA11_MOUSE] Involved in the presentation of foreign antigens to the immune system. [B2MG_MOUSE] Component of the class I major histocompatibility complex (MHC). Involved in the presentation of peptide antigens to the immune system. Publication Abstract from PubMedInfluenza A virus-specific CD8(+) cytotoxic T lymphocytes (CTLs) provide a degree of cross-strain protection that is potentially subverted by mutation. Here we describe the sequential emergence of such variants within CTL epitopes for a persistently infected, immunocompromised infant. Further analysis in immunodeficient and wild-type mice supports the view that CTL escape variants arise frequently in influenza, accumulate with time and revert in the absence of immune pressure under MHCI-mismatched conditions. Viral fitness, the abundance of endogenous CD8(+) T cell responses and T cell receptor repertoire diversity influence the nature of these de novo mutants. Structural characterization of dominant escape variants shows how the peptide-MHCI interaction is modified to affect variant-MHCI stability. The mechanism of influenza virus escape thus looks comparable to that recognized for chronic RNA viruses like HIV and HCV, suggesting that immunocompromised patients with prolonged viral infection could have an important part in the emergence of influenza quasispecies. Acute emergence and reversion of influenza A virus quasispecies within CD8(+) T cell antigenic peptides.,Valkenburg SA, Quinones-Parra S, Gras S, Komadina N, McVernon J, Wang Z, Halim H, Iannello P, Cole C, Laurie K, Kelso A, Rossjohn J, Doherty PC, Turner SJ, Kedzierska K Nat Commun. 2013 Oct 30;4:2663. doi: 10.1038/ncomms3663. PMID:24173108[1] From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine. See AlsoReferences
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