Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages.

Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages. Research Abstract Details 

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Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages. Abstract Text:

Swamy Kumar Polumuri,Vladimir Y Toshchakov,Stefanie N Vogel,

Ligation of FcgammaR concurrent with LPS stimulation of murine macrophages results in decreased IL-12 and increased IL-10 production. Because PI3K deficiency has been associated with increased IL-12, we hypothesized that PI3K was central to the anti-inflammatory effect of FcgammaR ligation on TLR-induced IL-12. FcgammaR ligation of macrophages increased pAKT, a correlate of PI3K activity, above levels induced by TLR4 or TLR2 agonists. This increase was blocked by PI3K inhibitors, wortmannin or LY294002, as was the effect of FcgammaR ligation on TLR-induced IL-12 and IL-10. LPS-induced binding of NF-kappaB to the IL-12 p40 promoter NF-kappaB-binding site was not affected by FcgammaR ligation at 1 h; however, by 4 h, NF-kappaB binding was markedly inhibited, confirmed in situ by chromatin immunoprecipitation analysis. This effect was wortmannin sensitive. Although TLR-induced IkappaBalpha degradation was not affected by FcgammaR ligation, IkappaBalpha accumulated in the nuclei of cells treated with LPS and FcgammaR ligation for 4 h, and was blocked by PI3K inhibitors. LPS-induced IFN regulatory factor-8/IFN consensus sequence-binding protein mRNA, and an IFN regulatory factor-8-dependent gene, Nos2, were inhibited by concurrent FcgammaR ligation, and this was also reversed by wortmannin. Thus, FcgammaR ligation modulates LPS-induced IL-12 via multiple PI3K-sensitive pathways that affect production, accumulation, and binding of key DNA-binding proteins required for IL-12 induction.

Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages. Publishing Authors By Initials

SK Polumuri,VY Toshchakov,SN Vogel,

For similar genetic processes: gene expression: transcription, genetic research abstracts see: genetic processes: gene expression: transcription, genetic research

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Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages. Journal Published:

PUBLICATION TYPE: Research Support, N.I.H., Extr

Journal: Journal of immunology (Baltimore, Md. : 1950)

VOLUME: 179

Page Numbers: 236-46

Journal Abbreviation: J. Immunol.

ISSN: 0022-1767

DAY: 1

MONTH: Jul

YEAR: 2007

Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages. Information

Number of References:

LANGUAGE: eng

NlmUniqueID: 2985117

Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages. Keywords Mesh Terms:

KEYWORDS: Transcription, Genetic

MESH TERMS: immunology

Chemical & Substance for Abstract: Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages. Information

Substance Name: Oncogene Protein v-akt

Registry Number: EC 2.7.1.37

Grant and Affiliation Information for Role of phosphatidylinositol-3 kinase in transcriptional regulation of TLR-induced IL-12 and IL-10 by Fc gamma receptor ligation in murine macrophages.

AFFILIATION: Department of Microbiology and Immunology, School of Medicine, University of Maryland, 660 West Redwood Street, Baltimore, MD 21201, USA.

Country: United States

AGENCY: United States NIAID

GRANT: AI 18797

ACRONYM: AI

MEDLINETA: J Immunol

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