Abstract
Nfil3 is viewed as an obligate transcription factor for NK cell development. However, mouse CMV (MCMV) infection recently was shown to bypass the requirement for Nfil3 by inducing the appearance of NK cells that express the MCMV-specific receptor Ly49H. Thus, signals transmitted by Ly49H and proinflammatory cytokines are sufficient to promote NK cell differentiation in the absence of Nfil3. In this study, we report that salivary gland (SG) NK cells develop in an Nfil3-independent fashion in the steady-state in the absence of MCMV or any infection. Moreover, we show that SG NK cells have an integrin profile reminiscent of tissue-resident lymphocytes and express TRAIL for killing target cells. These results demonstrate that SG NK cells, although related to conventional NK cells, are a distinct subset of innate lymphoid cells that deviates from the conventional developmental pathway, perhaps under the influence of tissue-specific factors.
Publication types
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Research Support, N.I.H., Extramural
MeSH terms
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Animals
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Basic-Leucine Zipper Transcription Factors / genetics
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Basic-Leucine Zipper Transcription Factors / immunology*
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Cell Differentiation / genetics
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Cell Differentiation / immunology*
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Herpesviridae Infections / genetics
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Herpesviridae Infections / immunology
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Herpesviridae Infections / pathology
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Killer Cells, Natural / immunology*
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Killer Cells, Natural / pathology
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Mice
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Mice, Knockout
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Muromegalovirus / immunology
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NK Cell Lectin-Like Receptor Subfamily A / genetics
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NK Cell Lectin-Like Receptor Subfamily A / immunology
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Organ Specificity / genetics
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Organ Specificity / immunology
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Salivary Glands / immunology*
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Salivary Glands / pathology
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TNF-Related Apoptosis-Inducing Ligand / genetics
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TNF-Related Apoptosis-Inducing Ligand / immunology
Substances
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Basic-Leucine Zipper Transcription Factors
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Klra8 protein, mouse
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NK Cell Lectin-Like Receptor Subfamily A
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Nfil3 protein, mouse
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TNF-Related Apoptosis-Inducing Ligand
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Tnfsf10 protein, mouse