Expression of m157, a murine cytomegalovirus-encoded putative major histocompatibility class I (MHC-I)-like protein, is independent of viral regulation of host MHC-I.
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Activation receptor-induced tolerance of mature NK cells in vivo requires signaling through the receptor and is reversibleLicensed and Unlicensed NK Cells: Differential Roles in Cancer and Viral ControlStructural elucidation of the m157 mouse cytomegalovirus ligand for Ly49 natural killer cell receptorsStreptolysin O clearance through sequestration into blebs that bud passively from the plasma membraneExpression of the RAE-1 family of stimulatory NK-cell ligands requires activation of the PI3K pathway during viral infection and transformation.Natural killer cell dependent within-host competition arises during multiple MCMV infection: consequences for viral transmission and evolution.Glycosylation contributes to variability in expression of murine cytomegalovirus m157 and enhances stability of interaction with the NK-cell receptor Ly49H.The Glycophosphatidylinositol Anchor of the MCMV Evasin, m157, Facilitates Optimal Cell Surface Expression and Ly49 Receptor Recognition.Acquisition of activation receptor ligand by trogocytosis renders NK cells hyporesponsive.A flow cytometry-based method for detecting antibody responses to murine cytomegalovirus infection.Mouse newborn cells allow highly productive mouse cytomegalovirus replication, constituting a novel convenient primary cell culture system.Characterization of murine cytomegalovirus m157 from infected cells and identification of critical residues mediating recognition by the NK cell receptor Ly49H.Tolerance of NK cells encountering their viral ligand during development.Continuous engagement of a self-specific activation receptor induces NK cell tolerance.CD28/B7-mediated co-stimulation is critical for early control of murine cytomegalovirus infectionImmune memory redefined: characterizing the longevity of natural killer cells.'Unlicensed' natural killer cells dominate the response to cytomegalovirus infection.Viral infection transiently reverses activation receptor-mediated NK cell hyporesponsiveness in an MHC class I-independent mechanism.Ly49H engagement compensates for the absence of type I interferon signaling in stimulating NK cell proliferation during murine cytomegalovirus infection.Feeling manipulated: cytomegalovirus immune manipulation.Origins of Natural Killer Cell Memory: Special Creation or Adaptive Evolution.Continuous CD27 triggering in vivo strongly reduces NK cell numbers.
P2860
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P2860
Expression of m157, a murine cytomegalovirus-encoded putative major histocompatibility class I (MHC-I)-like protein, is independent of viral regulation of host MHC-I.
description
2006 nî lūn-bûn
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2006 թուականի Յունուարին հրատարակուած գիտական յօդուած
@hyw
2006 թվականի հունվարին հրատարակված գիտական հոդված
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2006年の論文
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2006年論文
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2006年論文
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2006年論文
@zh-hk
2006年論文
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2006年論文
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2006年论文
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name
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@ast
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@en
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@nl
type
label
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@ast
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@en
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@nl
prefLabel
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@ast
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@en
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@nl
P2093
P2860
P1433
P1476
Expression of m157, a murine c ...... iral regulation of host MHC-I.
@en
P2093
Erika A Holroyd
Hamish R C Smith
Jeanette T Pingel
Sandeep K Tripathy
Wayne M Yokoyama
P2860
P304
P356
10.1128/JVI.80.1.545-550.2006
P407
P577
2006-01-01T00:00:00Z