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SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling
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SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling
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Journal Article
SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling
2017
Overview
Colonna and colleagues generate mice in which both type 1 innate lymphoid cells and natural killer cells selectively lack SMAD4, which promotes canonical signaling of all cytokines of the TGF-β family. Unexpectedly, SMAD4 deficiency does not visibly affect the differentiation of type 1 innate lymphoid cells but instead alters the phenotype of conventional natural killer cells.
Among the features that distinguish type 1 innate lymphoid cells (ILC1s) from natural killer (NK) cells is a gene signature indicative of 'imprinting' by cytokines of the TGF-β family. We studied mice in which ILC1s and NK cells lacked SMAD4, a signal transducer that facilitates the canonical signaling pathway common to all cytokines of the TGF-β family. While SMAD4 deficiency did not affect ILC1 differentiation, NK cells unexpectedly acquired an ILC1-like gene signature and were unable to control tumor metastasis or viral infection. Mechanistically, SMAD4 restrained non-canonical TGF-β signaling mediated by the cytokine receptor TGFβR1 in NK cells. NK cells from a SMAD4-deficient person affected by polyposis were also hyper-responsive to TGF-β. These results identify SMAD4 as a previously unknown regulator that restricts non-canonical TGF-β signaling in NK cells.
Publisher
Nature Publishing Group US
Subject
/ 13/106
/ 13/31
/ 13/95
/ 38
/ 38/61
/ 64
/ 64/60
/ Adenomatous Polyposis Coli - genetics
/ Adenomatous Polyposis Coli - immunology
/ Animals
/ Humans
/ Immunity, Innate - immunology
/ Immunologic Deficiency Syndromes - genetics
/ Immunologic Deficiency Syndromes - immunology
/ Killer Cells, Natural - cytology
/ Melanoma, Experimental - immunology
/ Mice
/ Reverse Transcriptase Polymerase Chain Reaction
