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This Article Full Text Full Text (PDF) Data Supplement All Versions of this Article: jimmunol.0901520v1 183/9/5830    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Google Scholar Articles by Geurs, T. L. Articles by French, A. R. PubMed PubMed Citation Articles by Geurs, T. L. Articles by French, A. R.

Ly49H Engagement Compensates for the Absence of Type I Interferon Signaling in Stimulating NK Cell Proliferation During Murine Cytomegalovirus Infection¹

Division of Pediatric Rheumatology, Department of Pediatrics, Washington University School of Medicine, St. Louis, MO 63110

NK cells vigorously proliferate during viral infections, resulting in an expanded pool of innate lymphocytes that are able to participate in early host defense. The relative contributions of cytokines and activation receptors in stimulating NK cell proliferation during viral infections are not well characterized. In this study, we demonstrated that signaling through the NK cell activation receptor Ly49H was able to compensate for the absence of cytokine stimulation in the preferential phase of viral-induced proliferation during murine cytomegalovirus infection. In the absence of type I IFN stimulation, NK cell proliferation was strongly biased toward cells expressing the Ly49H receptor, even at early time points when minimal preferential Ly49H-mediated proliferation was observed in wild-type mice. In the absence of effective Ly49H signaling or following infection with virus that did not express the ligand for Ly49H, no difference was observed in the proliferation of subsets of NK cells that either express or lack expression of Ly49H, although the overall proliferation of NK cells in IFNβR^–/– mice was substantially reduced. These results highlight the contribution of NK cell activation receptors in stimulating proliferation and subsequent expansion of NK cells that are able to recognize virally infected cells.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This research was supported by a National Institute of Allergy and Infectious Diseases K08 AI059083 Grant, a Basil O'Connor award from the March of Dimes, and the Washington University Child Health Research Center K12-HD01487 Grant.

² Address correspondence and reprint requests to Dr. Anthony R. French, Department of Pediatrics, Washington University, Box 8208, 660 South Euclid Avenue, St. Louis, MO 63110. E-mail address: french_a{at}kids.wustl.edu

³ Abbreviations used in this paper: MCMV, murine cytomegalovirus; wt, wild type; p.i., postinfection; MFI, mean fluorescence intensity.

⁴ The online version of this article contains supplemental material.