Natural Killer Cell Licensing During Viral Infection

Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 780)

Abstract

Natural Killer (NK) cell functionality is controlled by inhibitory receptors that recognize self-MHC class I. NK cells that do not interact with self-MHC class I are hypo-responsive to many stimuli and fail to reject MHC class I-deficient cells. Thus, although the mechanisms are unknown, interactions with MHC class I “licensed” NK cells respond efficiently. Surprisingly, these licensed NK cells fail to control viral infection. During mouse cytomegalovirus (MCMV) infection, SHP-1 signaling downstream of inhibitory receptors for MHC class I limits NK cell proliferation. Interactions with MHC class I prevent licensed NK cells from controlling of MCMV replication and pathogenesis; rather, it is the unlicensed NK cells that are not inhibited by self-MHC class I that efficiently control MCMV infection. Therefore, the licensing hypothesis is not sufficient to explain NK cell functionality during viral infection.

Keywords

Leukemia Influenza Integrin Inositol Listeria 

Notes

Acknowledgements

M.T.O is an Irvington Postdoctoral Fellow of the Cancer Research Institute. L.L.L. is an American Cancer Society Professor and is supported by NIH grants AI068129, CA095137, and AI066897.

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Copyright information

© Springer Science+Businees Media, LLC 2011

Authors and Affiliations

  1. 1.Department of Microbiology and Immunology and the Cancer Research InstituteUniversity of California San FranciscoSan FranciscoUSA

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