Early p38 Activation Regulated by MKP-1 Is Determinant for High Levels of IL-10 Expression Through TLR2 Activation.
Animals
Cells, Cultured
Cytokines
/ genetics
Diglycerides
/ pharmacology
Dual Specificity Phosphatase 1
/ genetics
Enzyme Activation
/ immunology
Gene Expression
/ drug effects
Interleukin-10
/ genetics
Lipopeptides
/ pharmacology
Lipopolysaccharides
/ pharmacology
Macrophages
/ drug effects
Mice
Mice, Inbred C57BL
Mice, Knockout
Oligopeptides
/ pharmacology
Phosphorylation
/ drug effects
RAW 264.7 Cells
Toll-Like Receptor 2
/ genetics
Toll-Like Receptor 4
/ genetics
p38 Mitogen-Activated Protein Kinases
/ immunology
MAPK signaling
cytokines
innate immunity
macrophages
toll-like receptors
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2021
2021
Historique:
received:
28
01
2021
accepted:
07
06
2021
entrez:
8
7
2021
pubmed:
9
7
2021
medline:
21
10
2021
Statut:
epublish
Résumé
Toll-like receptors (TLRs) play a crucial role in the recognition of pathogen-derived components as a first line of defense against infections. It has been suggested that depending on the nature of the pathogens, TLRs activation induce a distinct cytokine profile that may contribute to the polarization of the acquired immune response. Here, we investigated the early MAPK signaling activation
Identifiants
pubmed: 34234775
doi: 10.3389/fimmu.2021.660065
pmc: PMC8256158
doi:
Substances chimiques
Cytokines
0
Diglycerides
0
FSL-1 lipoprotein, synthetic
0
Lipopeptides
0
Lipopolysaccharides
0
Oligopeptides
0
Pam(3)CSK(4) peptide
0
Toll-Like Receptor 2
0
Toll-Like Receptor 4
0
Interleukin-10
130068-27-8
p38 Mitogen-Activated Protein Kinases
EC 2.7.11.24
Dual Specificity Phosphatase 1
EC 3.1.3.48
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
660065Informations de copyright
Copyright © 2021 Francisco, Arranz, Merino, Punzón, Perona and Fresno.
Déclaration de conflit d'intérêts
The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Références
PLoS One. 2009;4(5):e5601
pubmed: 19440307
Nat Immunol. 2008 Sep;9(9):1019-27
pubmed: 18677317
Cell Signal. 2007 Jul;19(7):1372-82
pubmed: 17512700
Proc Natl Acad Sci U S A. 2006 Feb 14;103(7):2274-9
pubmed: 16461893
Nat Immunol. 2008 Sep;9(9):1028-36
pubmed: 18690222
Nat Rev Drug Discov. 2007 May;6(5):391-403
pubmed: 17473844
Immunity. 2011 May 27;34(5):637-50
pubmed: 21616434
J Biol Chem. 2003 Feb 21;278(8):5597-604
pubmed: 12493739
Nat Rev Immunol. 2007 Mar;7(3):202-12
pubmed: 17318231
Nat Rev Immunol. 2004 Jul;4(7):499-511
pubmed: 15229469
J Exp Med. 2006 Jan 23;203(1):15-20
pubmed: 16380512
J Immunol. 2004 Mar 15;172(6):3712-8
pubmed: 15004175
Genes Dev. 2005 Nov 15;19(22):2668-81
pubmed: 16260493
Curr Opin Pharmacol. 2006 Aug;6(4):379-86
pubmed: 16713356
J Immunol. 2004 Dec 15;173(12):7548-55
pubmed: 15585882
Cell. 2007 Sep 21;130(6):1071-82
pubmed: 17889651
Science. 1999 Dec 24;286(5449):2514-7
pubmed: 10617468
J Clin Invest. 2006 Apr;116(4):916-28
pubmed: 16543948
J Biol Chem. 2001 Oct 5;276(40):37692-9
pubmed: 11477091
Int J Mol Sci. 2019 Sep 06;20(18):
pubmed: 31489884
J Biol Chem. 2005 Mar 4;280(9):8101-8
pubmed: 15590669
Annu Rev Immunol. 2002;20:197-216
pubmed: 11861602
J Exp Med. 2006 Jan 23;203(1):131-40
pubmed: 16380513
Immunity. 2009 Dec 18;31(6):873-84
pubmed: 19931471
Adv Immunol. 2011;109:87-124
pubmed: 21569913
Annu Rev Immunol. 2002;20:55-72
pubmed: 11861597
J Immunol. 2003 Nov 15;171(10):4984-9
pubmed: 14607893
J Biol Chem. 2001 Apr 27;276(17):13664-74
pubmed: 11278848
Infect Immun. 2015 Jun;83(6):2242-54
pubmed: 25776754
Infect Immun. 2001 Mar;69(3):1477-82
pubmed: 11179315