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IκB_NS-deficiency protects mice from fatal Listeria monocytogenes infection by blunting pro-inflammatory signature in Ly6C^high monocytes and preventing exaggerated innate immune responses.

ABSTRACT: IκB proteins regulate the inhibition and activation of NF-κB transcription factor complexes. While classical IκB proteins keep NF-κB complexes inactive in the cytoplasm, atypical IκB proteins act on activated NF-κB complexes located in the nucleus. Most of the knowledge regarding the function of IκB proteins has been collected in vitro, while far less is known regarding their impact on activation and regulation of immune responses during in vivo infections. Combining in vivo Listeria monocytogenes (Lm) infection with comparative ex vivo transcriptional profiling of the hepatic response to the pathogen we observed that in contrast to wild type mice that mounted a robust inflammatory response, IκB_NS-deficiency was generally associated with a transcripti

SUBMITTER: Frentzel S

PROVIDER: S-EPMC9813228 | biostudies-literature | 2022

REPOSITORIES: biostudies-literature

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Dataset Information

IκB_NS-deficiency protects mice from fatal Listeria monocytogenes infection by blunting pro-inflammatory signature in Ly6C^high monocytes and preventing exaggerated innate immune responses.

OmicsDI is part of the ELIXIR infrastructure

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Dataset Information

IκBNS-deficiency protects mice from fatal Listeria monocytogenes infection by blunting pro-inflammatory signature in Ly6Chigh monocytes and preventing exaggerated innate immune responses.

OmicsDI is part of the ELIXIR infrastructure

Tweets

IκB_NS-deficiency protects mice from fatal Listeria monocytogenes infection by blunting pro-inflammatory signature in Ly6C^high monocytes and preventing exaggerated innate immune responses.