C-Reactive Protein Controls IL-23 Production by Human Monocytes

C-reactive protein (CRP) is an acute-phase protein in humans that is produced in high quantities by the liver upon infection and under inflammatory conditions. Although CRP is commonly used as a marker of inflammation, CRP can also directly contribute to inflammation by eliciting pro-inflammatory cy...

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Autores principales: Chiara E. Geyer, Melissa Newling, Lathees Sritharan, Guillermo R. Griffith, Hung-Jen Chen, Dominique L. P. Baeten, Jeroen den Dunnen
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Publicado: MDPI AG 2021
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Acceso en línea:https://doaj.org/article/7100eea814c24301a1c161057fb9f7a5
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spelling oai:doaj.org-article:7100eea814c24301a1c161057fb9f7a52021-11-11T17:06:48ZC-Reactive Protein Controls IL-23 Production by Human Monocytes10.3390/ijms2221116381422-00671661-6596https://doaj.org/article/7100eea814c24301a1c161057fb9f7a52021-10-01T00:00:00Zhttps://www.mdpi.com/1422-0067/22/21/11638https://doaj.org/toc/1661-6596https://doaj.org/toc/1422-0067C-reactive protein (CRP) is an acute-phase protein in humans that is produced in high quantities by the liver upon infection and under inflammatory conditions. Although CRP is commonly used as a marker of inflammation, CRP can also directly contribute to inflammation by eliciting pro-inflammatory cytokine production by immune cells. Since CRP is highly elevated in serum under inflammatory conditions, we have studied the CRP-induced cytokine profile of human monocytes, one of the main innate immune cell populations in blood. We identified that CRP is relatively unique in its capacity to induce production of the pro-inflammatory cytokine IL-23, which was in stark contrast to a wide panel of pattern recognition receptor (PRR) ligands. We show that CRP-induced IL-23 production was mediated at the level of gene transcription, since CRP particularly promoted gene transcription of <i>IL23A</i> (encoding IL-23p19) instead of <i>IL12A</i> (encoding IL-12p35), while PRR ligands induce the opposite response. Interestingly, when CRP stimulation was combined with PRR ligand stimulation, as for example, occurs in the context of sepsis, IL-23 production by monocytes was strongly reduced. Combined, these data identify CRP as a unique individual ligand to induce IL-23 production by monocytes, which may contribute to shaping systemic immune responses under inflammatory conditions.Chiara E. GeyerMelissa NewlingLathees SritharanGuillermo R. GriffithHung-Jen ChenDominique L. P. BaetenJeroen den DunnenMDPI AGarticleC-reactive proteinIL-23inflammationmonocyteFc receptorSepsisBiology (General)QH301-705.5ChemistryQD1-999ENInternational Journal of Molecular Sciences, Vol 22, Iss 11638, p 11638 (2021)
institution DOAJ
collection DOAJ
language EN
topic C-reactive protein
IL-23
inflammation
monocyte
Fc receptor
Sepsis
Biology (General)
QH301-705.5
Chemistry
QD1-999
spellingShingle C-reactive protein
IL-23
inflammation
monocyte
Fc receptor
Sepsis
Biology (General)
QH301-705.5
Chemistry
QD1-999
Chiara E. Geyer
Melissa Newling
Lathees Sritharan
Guillermo R. Griffith
Hung-Jen Chen
Dominique L. P. Baeten
Jeroen den Dunnen
C-Reactive Protein Controls IL-23 Production by Human Monocytes
description C-reactive protein (CRP) is an acute-phase protein in humans that is produced in high quantities by the liver upon infection and under inflammatory conditions. Although CRP is commonly used as a marker of inflammation, CRP can also directly contribute to inflammation by eliciting pro-inflammatory cytokine production by immune cells. Since CRP is highly elevated in serum under inflammatory conditions, we have studied the CRP-induced cytokine profile of human monocytes, one of the main innate immune cell populations in blood. We identified that CRP is relatively unique in its capacity to induce production of the pro-inflammatory cytokine IL-23, which was in stark contrast to a wide panel of pattern recognition receptor (PRR) ligands. We show that CRP-induced IL-23 production was mediated at the level of gene transcription, since CRP particularly promoted gene transcription of <i>IL23A</i> (encoding IL-23p19) instead of <i>IL12A</i> (encoding IL-12p35), while PRR ligands induce the opposite response. Interestingly, when CRP stimulation was combined with PRR ligand stimulation, as for example, occurs in the context of sepsis, IL-23 production by monocytes was strongly reduced. Combined, these data identify CRP as a unique individual ligand to induce IL-23 production by monocytes, which may contribute to shaping systemic immune responses under inflammatory conditions.
format article
author Chiara E. Geyer
Melissa Newling
Lathees Sritharan
Guillermo R. Griffith
Hung-Jen Chen
Dominique L. P. Baeten
Jeroen den Dunnen
author_facet Chiara E. Geyer
Melissa Newling
Lathees Sritharan
Guillermo R. Griffith
Hung-Jen Chen
Dominique L. P. Baeten
Jeroen den Dunnen
author_sort Chiara E. Geyer
title C-Reactive Protein Controls IL-23 Production by Human Monocytes
title_short C-Reactive Protein Controls IL-23 Production by Human Monocytes
title_full C-Reactive Protein Controls IL-23 Production by Human Monocytes
title_fullStr C-Reactive Protein Controls IL-23 Production by Human Monocytes
title_full_unstemmed C-Reactive Protein Controls IL-23 Production by Human Monocytes
title_sort c-reactive protein controls il-23 production by human monocytes
publisher MDPI AG
publishDate 2021
url https://doaj.org/article/7100eea814c24301a1c161057fb9f7a5
work_keys_str_mv AT chiaraegeyer creactiveproteincontrolsil23productionbyhumanmonocytes
AT melissanewling creactiveproteincontrolsil23productionbyhumanmonocytes
AT latheessritharan creactiveproteincontrolsil23productionbyhumanmonocytes
AT guillermorgriffith creactiveproteincontrolsil23productionbyhumanmonocytes
AT hungjenchen creactiveproteincontrolsil23productionbyhumanmonocytes
AT dominiquelpbaeten creactiveproteincontrolsil23productionbyhumanmonocytes
AT jeroendendunnen creactiveproteincontrolsil23productionbyhumanmonocytes
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