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J Immunol. 2015 Jun 15;194(12):5948-52. doi: 10.4049/jimmunol.1500424. Epub 2015 Apr 29.

IL-33 receptor ST2 amplifies the expansion of NK cells and enhances host defense during mouse cytomegalovirus infection.

Author information

1
Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143; Life Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba, Ibaraki 305-8577, Japan; and.
2
Centre National de la Recherche Scientifique and Université de Toulouse, Institut de Pharmacologie et de Biologie Structurale, F-31077 Toulouse, France.
3
Department of Microbiology and Immunology and the Cancer Research Institute, University of California, San Francisco, San Francisco, CA 94143; Lewis.Lanier@ucsf.edu.

Abstract

NK cells provide important host defense against viruses and can differentiate into self-renewing memory NK cells after infection, alloantigen stimulation, and cytokine stimulation. In this study, we investigated the role of the IL-33 receptor ST2 in the differentiation of NK cells during mouse CMV (MCMV) infection. Although ST2-deficient (Il1rl1 (-/-)) Ly49H(+) NK cells develop normally and differentiate into memory cells after MCMV infection, naive and memory Il1rl1 (-/-) Ly49H(+) NK cells exhibited profound defects in MCMV-specific expansion, resulting in impaired protection against MCMV challenge. Additionally, IL-33 enhanced m157 Ag-specific proliferation of Ly49H(+) NK cells in vitro. Thus, an IL-33/ST2 signaling axis in NK cells contributes to host defense against MCMV.

PMID:
25926677
PMCID:
PMC4458425
DOI:
10.4049/jimmunol.1500424
[Indexed for MEDLINE]
Free PMC Article

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