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Mettl3-mediated mRNA m6A methylation promotes dendritic cell activation
N6-methyladenosine (m 6 A) modification plays important roles in various cellular responses by regulating mRNA biology. However, how m 6 A modification is involved in innate immunity via affecting the translation of immune transcripts remains to be further investigated. Here we report that RNA methy...
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| Published in: | Nature communications 2019-04, Vol.10 (1), p.1898-1898, Article 1898 |
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| creator | Wang, Huamin Hu, Xiang Huang, Mingyan Liu, Juan Gu, Yan Ma, Lijia Zhou, Qi Cao, Xuetao |
| description | N6-methyladenosine (m
6
A) modification plays important roles in various cellular responses by regulating mRNA biology. However, how m
6
A modification is involved in innate immunity via affecting the translation of immune transcripts remains to be further investigated. Here we report that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function. Specific depletion of
Mettl3
in DC resulted in impaired phenotypic and functional maturation of DC, with decreased expression of co-stimulatory molecules CD40, CD80 and cytokine IL-12, and reduced ability to stimulate T cell responses both in vitro and in vivo. Mechanistically, Mettl3-mediated m
6
A of CD40, CD80 and TLR4 signaling adaptor Tirap transcripts enhanced their translation in DC for stimulating T cell activation, and strengthening TLR4/NF-κB signaling-induced cytokine production. Our findings identify a new role for Mettl3-mediated m
6
A modification in increasing translation of certain immune transcripts for physiological promotion of DC activation and DC-based T cell response.
Here the authors examine how m
6
A modification is involved in innate immunity. They show that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function, and in promoting DC-based T cells responses. |
| doi_str_mv | 10.1038/s41467-019-09903-6 |
| format | article |
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6
A) modification plays important roles in various cellular responses by regulating mRNA biology. However, how m
6
A modification is involved in innate immunity via affecting the translation of immune transcripts remains to be further investigated. Here we report that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function. Specific depletion of
Mettl3
in DC resulted in impaired phenotypic and functional maturation of DC, with decreased expression of co-stimulatory molecules CD40, CD80 and cytokine IL-12, and reduced ability to stimulate T cell responses both in vitro and in vivo. Mechanistically, Mettl3-mediated m
6
A of CD40, CD80 and TLR4 signaling adaptor Tirap transcripts enhanced their translation in DC for stimulating T cell activation, and strengthening TLR4/NF-κB signaling-induced cytokine production. Our findings identify a new role for Mettl3-mediated m
6
A modification in increasing translation of certain immune transcripts for physiological promotion of DC activation and DC-based T cell response.
Here the authors examine how m
6
A modification is involved in innate immunity. They show that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function, and in promoting DC-based T cells responses.</description><identifier>ISSN: 2041-1723</identifier><identifier>EISSN: 2041-1723</identifier><identifier>DOI: 10.1038/s41467-019-09903-6</identifier><identifier>PMID: 31015515</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>49 ; 49/91 ; 631/250/21/1293 ; 631/250/2502/2170 ; 631/80/86 ; CD40 antigen ; CD80 antigen ; Cell activation ; Cytokines ; Dendritic cells ; Dendritic structure ; Depletion ; Humanities and Social Sciences ; Immunity ; Innate immunity ; Interleukin 12 ; Lymphocytes ; Lymphocytes T ; Methylation ; multidisciplinary ; N6-methyladenosine ; NF-κB protein ; Science ; Science (multidisciplinary) ; Signaling ; TLR4 protein ; Toll-like receptors ; Translation</subject><ispartof>Nature communications, 2019-04, Vol.10 (1), p.1898-1898, Article 1898</ispartof><rights>The Author(s) 2019</rights><rights>The Author(s) 2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4286-f32ee1729dae501f12212951a536eeb25ac14064e5e985002088d107d4fe1a0f3</citedby><cites>FETCH-LOGICAL-c4286-f32ee1729dae501f12212951a536eeb25ac14064e5e985002088d107d4fe1a0f3</cites><orcidid>0000-0001-9677-7647 ; 0000-0001-5120-1222 ; 0000-0002-6549-9362</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2393002651/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2393002651?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,37013,44590,53791,53793,74998</link.rule.ids></links><search><creatorcontrib>Wang, Huamin</creatorcontrib><creatorcontrib>Hu, Xiang</creatorcontrib><creatorcontrib>Huang, Mingyan</creatorcontrib><creatorcontrib>Liu, Juan</creatorcontrib><creatorcontrib>Gu, Yan</creatorcontrib><creatorcontrib>Ma, Lijia</creatorcontrib><creatorcontrib>Zhou, Qi</creatorcontrib><creatorcontrib>Cao, Xuetao</creatorcontrib><title>Mettl3-mediated mRNA m6A methylation promotes dendritic cell activation</title><title>Nature communications</title><addtitle>Nat Commun</addtitle><description>N6-methyladenosine (m
6
A) modification plays important roles in various cellular responses by regulating mRNA biology. However, how m
6
A modification is involved in innate immunity via affecting the translation of immune transcripts remains to be further investigated. Here we report that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function. Specific depletion of
Mettl3
in DC resulted in impaired phenotypic and functional maturation of DC, with decreased expression of co-stimulatory molecules CD40, CD80 and cytokine IL-12, and reduced ability to stimulate T cell responses both in vitro and in vivo. Mechanistically, Mettl3-mediated m
6
A of CD40, CD80 and TLR4 signaling adaptor Tirap transcripts enhanced their translation in DC for stimulating T cell activation, and strengthening TLR4/NF-κB signaling-induced cytokine production. Our findings identify a new role for Mettl3-mediated m
6
A modification in increasing translation of certain immune transcripts for physiological promotion of DC activation and DC-based T cell response.
Here the authors examine how m
6
A modification is involved in innate immunity. They show that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function, and in promoting DC-based T cells responses.</description><subject>49</subject><subject>49/91</subject><subject>631/250/21/1293</subject><subject>631/250/2502/2170</subject><subject>631/80/86</subject><subject>CD40 antigen</subject><subject>CD80 antigen</subject><subject>Cell activation</subject><subject>Cytokines</subject><subject>Dendritic cells</subject><subject>Dendritic structure</subject><subject>Depletion</subject><subject>Humanities and Social Sciences</subject><subject>Immunity</subject><subject>Innate immunity</subject><subject>Interleukin 12</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Methylation</subject><subject>multidisciplinary</subject><subject>N6-methyladenosine</subject><subject>NF-κB protein</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signaling</subject><subject>TLR4 protein</subject><subject>Toll-like 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Nature communications</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Huamin</au><au>Hu, Xiang</au><au>Huang, Mingyan</au><au>Liu, Juan</au><au>Gu, Yan</au><au>Ma, Lijia</au><au>Zhou, Qi</au><au>Cao, Xuetao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mettl3-mediated mRNA m6A methylation promotes dendritic cell activation</atitle><jtitle>Nature communications</jtitle><stitle>Nat Commun</stitle><date>2019-04-23</date><risdate>2019</risdate><volume>10</volume><issue>1</issue><spage>1898</spage><epage>1898</epage><pages>1898-1898</pages><artnum>1898</artnum><issn>2041-1723</issn><eissn>2041-1723</eissn><abstract>N6-methyladenosine (m
6
A) modification plays important roles in various cellular responses by regulating mRNA biology. However, how m
6
A modification is involved in innate immunity via affecting the translation of immune transcripts remains to be further investigated. Here we report that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function. Specific depletion of
Mettl3
in DC resulted in impaired phenotypic and functional maturation of DC, with decreased expression of co-stimulatory molecules CD40, CD80 and cytokine IL-12, and reduced ability to stimulate T cell responses both in vitro and in vivo. Mechanistically, Mettl3-mediated m
6
A of CD40, CD80 and TLR4 signaling adaptor Tirap transcripts enhanced their translation in DC for stimulating T cell activation, and strengthening TLR4/NF-κB signaling-induced cytokine production. Our findings identify a new role for Mettl3-mediated m
6
A modification in increasing translation of certain immune transcripts for physiological promotion of DC activation and DC-based T cell response.
Here the authors examine how m
6
A modification is involved in innate immunity. They show that RNA methyltransferase Mettl3-mediated mRNA m
6
A methylation promotes dendritic cell (DC) activation and function, and in promoting DC-based T cells responses.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31015515</pmid><doi>10.1038/s41467-019-09903-6</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0001-9677-7647</orcidid><orcidid>https://orcid.org/0000-0001-5120-1222</orcidid><orcidid>https://orcid.org/0000-0002-6549-9362</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | 49 49/91 631/250/21/1293 631/250/2502/2170 631/80/86 CD40 antigen CD80 antigen Cell activation Cytokines Dendritic cells Dendritic structure Depletion Humanities and Social Sciences Immunity Innate immunity Interleukin 12 Lymphocytes Lymphocytes T Methylation multidisciplinary N6-methyladenosine NF-κB protein Science Science (multidisciplinary) Signaling TLR4 protein Toll-like receptors Translation |
| title | Mettl3-mediated mRNA m6A methylation promotes dendritic cell activation |
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