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Journal Abstract Search

209 related items for PubMed ID: 24873973

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  • 3. Viral infection transiently reverses activation receptor-mediated NK cell hyporesponsiveness in an MHC class I-independent mechanism.
    Mazumdar B, Bolanos FD, Tripathy SK.
    Eur J Immunol; 2013 May; 43(5):1345-55. PubMed ID: 23440763
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  • 4. Critical residues at the Ly49 natural killer receptor's homodimer interface determine functional recognition of m157, a mouse cytomegalovirus MHC class I-like protein.
    Kielczewska A, Kim HS, Lanier LL, Dimasi N, Vidal SM.
    J Immunol; 2007 Jan 01; 178(1):369-77. PubMed ID: 17182575
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  • 6. Viral MHC class I-like molecule allows evasion of NK cell effector responses in vivo.
    Pyzik M, Dumaine A, Charbonneau B, Fodil-Cornu N, Jonjic S, Vidal SM.
    J Immunol; 2014 Dec 15; 193(12):6061-9. PubMed ID: 25392524
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  • 13. Ly49H signaling through DAP10 is essential for optimal natural killer cell responses to mouse cytomegalovirus infection.
    Orr MT, Sun JC, Hesslein DG, Arase H, Phillips JH, Takai T, Lanier LL.
    J Exp Med; 2009 Apr 13; 206(4):807-17. PubMed ID: 19332875
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  • 17. Distinct MHC class I-dependent NK cell-activating receptors control cytomegalovirus infection in different mouse strains.
    Pyzik M, Charbonneau B, Gendron-Pontbriand EM, Babić M, Krmpotić A, Jonjić S, Vidal SM.
    J Exp Med; 2011 May 09; 208(5):1105-17. PubMed ID: 21518798
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  • 20. Characterization of murine cytomegalovirus m157 from infected cells and identification of critical residues mediating recognition by the NK cell receptor Ly49H.
    Davis AH, Guseva NV, Ball BL, Heusel JW.
    J Immunol; 2008 Jul 01; 181(1):265-75. PubMed ID: 18566392
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