Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons

Type I interferons (IFNs) are essential for anti-viral immunity, but often impair protective immune responses during bacterial infections. An important question is how type I IFNs are strongly induced during viral infections, and yet are appropriately restrained during bacterial infections. The Supe...
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Autor*in:	Daisy X Ji [verfasserIn] Kristen C Witt [verfasserIn] Dmitri I Kotov [verfasserIn] Shally R Margolis [verfasserIn] Alexander Louie [verfasserIn] Victoria Chevée [verfasserIn] Katherine J Chen [verfasserIn] Moritz M Gaidt [verfasserIn] Harmandeep S Dhaliwal [verfasserIn] Angus Y Lee [verfasserIn] Stephen L Nishimura [verfasserIn] Dario S Zamboni [verfasserIn] Igor Kramnik [verfasserIn] Daniel A Portnoy [verfasserIn] K Heran Darwin [verfasserIn] Russell E Vance [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	mycobacterium tuberculosis legionella pneumophila type i interferon

Übergeordnetes Werk:	In: eLife - eLife Sciences Publications Ltd, 2013, 10(2021)
Übergeordnetes Werk:	volume:10 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.7554/eLife.67290

Katalog-ID:	DOAJ022174443

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spelling	10.7554/eLife.67290 doi (DE-627)DOAJ022174443 (DE-599)DOAJa13a048f3761473cb07137e4ffca8ea4 DE-627 ger DE-627 rakwb eng QH301-705.5 Daisy X Ji verfasserin aut Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Type I interferons (IFNs) are essential for anti-viral immunity, but often impair protective immune responses during bacterial infections. An important question is how type I IFNs are strongly induced during viral infections, and yet are appropriately restrained during bacterial infections. The Super susceptibility to tuberculosis 1 (Sst1) locus in mice confers resistance to diverse bacterial infections. Here we provide evidence that Sp140 is a gene encoded within the Sst1 locus that represses type I IFN transcription during bacterial infections. We generated Sp140–/– mice and found that they are susceptible to infection by Legionella pneumophila and Mycobacterium tuberculosis. Susceptibility of Sp140–/– mice to bacterial infection was rescued by crosses to mice lacking the type I IFN receptor (Ifnar–/–). Our results implicate Sp140 as an important negative regulator of type I IFNs that is essential for resistance to bacterial infections. mycobacterium tuberculosis legionella pneumophila type i interferon Medicine R Science Q Biology (General) Kristen C Witt verfasserin aut Dmitri I Kotov verfasserin aut Shally R Margolis verfasserin aut Alexander Louie verfasserin aut Victoria Chevée verfasserin aut Katherine J Chen verfasserin aut Moritz M Gaidt verfasserin aut Harmandeep S Dhaliwal verfasserin aut Angus Y Lee verfasserin aut Stephen L Nishimura verfasserin aut Dario S Zamboni verfasserin aut Igor Kramnik verfasserin aut Daniel A Portnoy verfasserin aut K Heran Darwin verfasserin aut Russell E Vance verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 10(2021) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:10 year:2021 https://doi.org/10.7554/eLife.67290 kostenfrei https://doaj.org/article/a13a048f3761473cb07137e4ffca8ea4 kostenfrei https://elifesciences.org/articles/67290 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2021
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allfieldsSound	10.7554/eLife.67290 doi (DE-627)DOAJ022174443 (DE-599)DOAJa13a048f3761473cb07137e4ffca8ea4 DE-627 ger DE-627 rakwb eng QH301-705.5 Daisy X Ji verfasserin aut Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Type I interferons (IFNs) are essential for anti-viral immunity, but often impair protective immune responses during bacterial infections. An important question is how type I IFNs are strongly induced during viral infections, and yet are appropriately restrained during bacterial infections. The Super susceptibility to tuberculosis 1 (Sst1) locus in mice confers resistance to diverse bacterial infections. Here we provide evidence that Sp140 is a gene encoded within the Sst1 locus that represses type I IFN transcription during bacterial infections. We generated Sp140–/– mice and found that they are susceptible to infection by Legionella pneumophila and Mycobacterium tuberculosis. Susceptibility of Sp140–/– mice to bacterial infection was rescued by crosses to mice lacking the type I IFN receptor (Ifnar–/–). Our results implicate Sp140 as an important negative regulator of type I IFNs that is essential for resistance to bacterial infections. mycobacterium tuberculosis legionella pneumophila type i interferon Medicine R Science Q Biology (General) Kristen C Witt verfasserin aut Dmitri I Kotov verfasserin aut Shally R Margolis verfasserin aut Alexander Louie verfasserin aut Victoria Chevée verfasserin aut Katherine J Chen verfasserin aut Moritz M Gaidt verfasserin aut Harmandeep S Dhaliwal verfasserin aut Angus Y Lee verfasserin aut Stephen L Nishimura verfasserin aut Dario S Zamboni verfasserin aut Igor Kramnik verfasserin aut Daniel A Portnoy verfasserin aut K Heran Darwin verfasserin aut Russell E Vance verfasserin aut In eLife eLife Sciences Publications Ltd, 2013 10(2021) (DE-627)728518384 (DE-600)2687154-3 2050084X nnns volume:10 year:2021 https://doi.org/10.7554/eLife.67290 kostenfrei https://doaj.org/article/a13a048f3761473cb07137e4ffca8ea4 kostenfrei https://elifesciences.org/articles/67290 kostenfrei https://doaj.org/toc/2050-084X Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4335 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 10 2021
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authorswithroles_txt_mv	Daisy X Ji @@aut@@ Kristen C Witt @@aut@@ Dmitri I Kotov @@aut@@ Shally R Margolis @@aut@@ Alexander Louie @@aut@@ Victoria Chevée @@aut@@ Katherine J Chen @@aut@@ Moritz M Gaidt @@aut@@ Harmandeep S Dhaliwal @@aut@@ Angus Y Lee @@aut@@ Stephen L Nishimura @@aut@@ Dario S Zamboni @@aut@@ Igor Kramnik @@aut@@ Daniel A Portnoy @@aut@@ K Heran Darwin @@aut@@ Russell E Vance @@aut@@
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callnumber-first	Q - Science
author	Daisy X Ji
spellingShingle	Daisy X Ji misc QH301-705.5 misc mycobacterium tuberculosis misc legionella pneumophila misc type i interferon misc Medicine misc R misc Science misc Q misc Biology (General) Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons
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topic_title	QH301-705.5 Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons mycobacterium tuberculosis legionella pneumophila type i interferon
topic	misc QH301-705.5 misc mycobacterium tuberculosis misc legionella pneumophila misc type i interferon misc Medicine misc R misc Science misc Q misc Biology (General)
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title	Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons
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title_full	Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons
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author_browse	Daisy X Ji Kristen C Witt Dmitri I Kotov Shally R Margolis Alexander Louie Victoria Chevée Katherine J Chen Moritz M Gaidt Harmandeep S Dhaliwal Angus Y Lee Stephen L Nishimura Dario S Zamboni Igor Kramnik Daniel A Portnoy K Heran Darwin Russell E Vance
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title_sort	role of the transcriptional regulator sp140 in resistance to bacterial infections via repression of type i interferons
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title_auth	Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons
abstract	Type I interferons (IFNs) are essential for anti-viral immunity, but often impair protective immune responses during bacterial infections. An important question is how type I IFNs are strongly induced during viral infections, and yet are appropriately restrained during bacterial infections. The Super susceptibility to tuberculosis 1 (Sst1) locus in mice confers resistance to diverse bacterial infections. Here we provide evidence that Sp140 is a gene encoded within the Sst1 locus that represses type I IFN transcription during bacterial infections. We generated Sp140–/– mice and found that they are susceptible to infection by Legionella pneumophila and Mycobacterium tuberculosis. Susceptibility of Sp140–/– mice to bacterial infection was rescued by crosses to mice lacking the type I IFN receptor (Ifnar–/–). Our results implicate Sp140 as an important negative regulator of type I IFNs that is essential for resistance to bacterial infections.
abstractGer	Type I interferons (IFNs) are essential for anti-viral immunity, but often impair protective immune responses during bacterial infections. An important question is how type I IFNs are strongly induced during viral infections, and yet are appropriately restrained during bacterial infections. The Super susceptibility to tuberculosis 1 (Sst1) locus in mice confers resistance to diverse bacterial infections. Here we provide evidence that Sp140 is a gene encoded within the Sst1 locus that represses type I IFN transcription during bacterial infections. We generated Sp140–/– mice and found that they are susceptible to infection by Legionella pneumophila and Mycobacterium tuberculosis. Susceptibility of Sp140–/– mice to bacterial infection was rescued by crosses to mice lacking the type I IFN receptor (Ifnar–/–). Our results implicate Sp140 as an important negative regulator of type I IFNs that is essential for resistance to bacterial infections.
abstract_unstemmed	Type I interferons (IFNs) are essential for anti-viral immunity, but often impair protective immune responses during bacterial infections. An important question is how type I IFNs are strongly induced during viral infections, and yet are appropriately restrained during bacterial infections. The Super susceptibility to tuberculosis 1 (Sst1) locus in mice confers resistance to diverse bacterial infections. Here we provide evidence that Sp140 is a gene encoded within the Sst1 locus that represses type I IFN transcription during bacterial infections. We generated Sp140–/– mice and found that they are susceptible to infection by Legionella pneumophila and Mycobacterium tuberculosis. Susceptibility of Sp140–/– mice to bacterial infection was rescued by crosses to mice lacking the type I IFN receptor (Ifnar–/–). Our results implicate Sp140 as an important negative regulator of type I IFNs that is essential for resistance to bacterial infections.
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title_short	Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons
url	https://doi.org/10.7554/eLife.67290 https://doaj.org/article/a13a048f3761473cb07137e4ffca8ea4 https://elifesciences.org/articles/67290 https://doaj.org/toc/2050-084X
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up_date	2024-07-04T00:30:51.144Z
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Role of the transcriptional regulator SP140 in resistance to bacterial infections via repression of type I interferons

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