MicroRNA-142 is critical for the homeostasis and function of type 1 innate lymphoid cells Journal Article


Authors: Berrien-Elliott, M. M.; Sun, Y.; Neal, C.; Ireland, A.; Trissal, M. C.; Sullivan, R. P.; Wagner, J. A.; Leong, J. W.; Wong, P.; Mah-Som, A. Y.; Wong, T. N.; Schappe, T.; Keppel, C. R.; Cortez, V. S.; Stamatiades, E. G.; Li, M. O.; Colonna, M.; Link, D. C.; French, A. R.; Cooper, M. A.; Wang, W. L.; Boldin, M. P.; Reddy, P.; Fehniger, T. A.
Article Title: MicroRNA-142 is critical for the homeostasis and function of type 1 innate lymphoid cells
Abstract: Natural killer (NK) cells are cytotoxic type 1 innate lymphoid cells (ILCs) that defend against viruses and mediate anti-tumor responses, yet mechanisms controlling their development and function remain incompletely understood. We hypothesized that the abundantly expressed microRNA-142 (miR-142) is a critical regulator of type 1 ILC biology. Interleukin-15 (IL-15) signaling induced miR-142 expression, whereas global and ILC-specific miR-142-deficient mice exhibited a cell-intrinsic loss of NK cells. Death of NK cells resulted from diminished IL-15 receptor signaling within miR-142-deficient mice, likely via reduced suppressor of cytokine signaling-1 (Socs1) regulation by miR-142-5p. ILCs persisting in Mir142−/− mice demonstrated increased expression of the miR-142-3p target αV integrin, which supported their survival. Global miR-142-deficient mice exhibited an expansion of ILC1-like cells concurrent with increased transforming growth factor-β (TGF-β) signaling. Further, miR-142-deficient mice had reduced NK-cell-dependent function and increased susceptibility to murine cytomegalovirus (MCMV) infection. Thus, miR-142 critically integrates environmental cues for proper type 1 ILC homeostasis and defense against viral infection. © 2019 Elsevier Inc.
Keywords: integrin; nk cells; il-15; murine cytomegalovirus; innate lymphoid cells; cytokine receptors; tissue resident; ilc1-like cells; microrna-142
Journal Title: Immunity
Volume: 51
Issue: 3
ISSN: 1074-7613
Publisher: Cell Press  
Date Published: 2019-09-17
Start Page: 479
End Page: 490.e6
Language: English
DOI: 10.1016/j.immuni.2019.06.016
PUBMED: 31402259
PROVIDER: scopus
PMCID: PMC6750984
DOI/URL:
Notes: Article -- Export Date: 1 October 2019 -- Source: Scopus
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  1. Ming Li
    111 Li