Document Detail


The regulation of Th1 responses by the p38 MAPK.
MedLine Citation:
PMID:  20937847     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
IL-12 is a dimeric cytokine that is produced primarily by APCs. In this study we examined the role that the p38 MAPKs (MAPK/p38) play in regulating IL-12 production. We show that inhibition of p38 dramatically increased IL-12 production upon stimulation, while decreasing TNF-α. This reciprocal effect on these two cytokines following MAPK/p38 inhibition occurred in many different APCs, following a variety of different stimuli. IL-12 production was also increased in macrophages treated with small interfering RNA to limit p38α expression, and in macrophages deficient in MKK3, a kinase upstream of p38. The increase in IL-12 production following MAPK/p38 inhibition appears to be due to enhanced IL-12 (p40) mRNA stability. We show that MAPK/p38 inhibition can promote Th1 immune responses and thereby enhance vaccine efficacy against leishmaniasis. In a mouse model of Leishmania major infection, vaccination with heat-killed L. major plus CpG and SB203580 elicited complete protection against infection compared with heat-killed L. major plus CpG without SB203580. Thus, this work suggests that MAPK/p38 inhibitors may be applied as adjuvants to bias immune responses and improve vaccinations against intracellular pathogens.
Authors:
Ziyan Yang; Xia Zhang; Patricia A Darrah; David M Mosser
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-10-11
Journal Detail:
Title:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  185     ISSN:  1550-6606     ISO Abbreviation:  J. Immunol.     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-04     Completed Date:  2010-12-02     Revised Date:  2011-09-26    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  6205-13     Citation Subset:  AIM; IM    
Affiliation:
Department of Cell Biology and Molecular Genetics, University of Maryland, College Park, MD 20742, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigen-Presenting Cells / immunology,  metabolism
Blotting, Western
Enzyme Inhibitors / pharmacology
Gene Expression Regulation / immunology*
Imidazoles / pharmacology
Interleukin-12 / biosynthesis*,  immunology
Leishmaniasis / immunology,  prevention & control
Leishmaniasis Vaccines / immunology*
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Mice, Knockout
Pyridines / pharmacology
RNA, Small Interfering
Reverse Transcriptase Polymerase Chain Reaction
Transfection
Tumor Necrosis Factor-alpha / biosynthesis,  immunology
p38 Mitogen-Activated Protein Kinases / immunology,  metabolism*
Grant Support
ID/Acronym/Agency:
AI55576/AI/NIAID NIH HHS; R01 AI049383-10/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Enzyme Inhibitors; 0/Imidazoles; 0/Leishmaniasis Vaccines; 0/Pyridines; 0/RNA, Small Interfering; 0/SB 203580; 0/Tumor Necrosis Factor-alpha; 187348-17-0/Interleukin-12; EC 2.7.11.24/p38 Mitogen-Activated Protein Kinases
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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