NDLI: The role of JAK-3 in regulating TLR-mediated inflammatory cytokine production in innate immune cells.

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The role of JAK-3 in regulating TLR-mediated inflammatory cytokine production in innate immune cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Zhou, Huaxin Brown, Jonathan Liang, Shuang Suttles, Jill Jotwani, Ravi Lamont, Richard J. Wang, Huizhi Gao, Shegan Scott, David A.
Description	Country affiliation: United States Author Affiliation: Wang H ( Oral Health and Systemic Disease Research Group, University of Louisville School of Dentistry, Louisville, KY 40202, USA. hhwang01@louisville.edu)
Abstract	The role of JAK-3 in TLR-mediated innate immune responses is poorly understood, although the suppressive function of JAK3 inhibition in adaptive immune response has been well studied. In this study, we found that JAK3 inhibition enhanced TLR-mediated immune responses by differentially regulating pro- and anti- inflammatory cytokine production in innate immune cells. Specifically, JAK3 inhibition by pharmacological inhibitors or specific small interfering RNA or JAK3 gene knockout resulted in an increase in TLR-mediated production of proinflammatory cytokines while concurrently decreasing the production of IL-10. Inhibition of JAK3 suppressed phosphorylation of PI3K downstream effectors including Akt, mammalian target of rapamycin complex 1, glycogen synthase kinase 3ß (GSK3ß), and CREB. Constitutive activation of Akt or inhibition of GSK3ß abrogated the capability of JAK3 inhibition to enhance proinflammatory cytokines and suppress IL-10 production. In contrast, inhibition of PI3K enhanced this regulatory ability of JAK3 in LPS-stimulated monocytes. At the transcriptional level, JAK3 knockout lead to the increased phosphorylation of STATs that could be attenuated by neutralization of de novo inflammatory cytokines. JAK3 inhibition exhibited a GSK3 activity-dependent ability to enhance phosphorylation levels and DNA binding of NF-κB p65. Moreover, JAK3 inhibition correlated with an increased CD4(+) T cell response. Additionally, higher neutrophil infiltration, IL-17 expression, and intestinal epithelium erosion were observed in JAK3 knockout mice. These findings demonstrate the negative regulatory function of JAK3 and elucidate the signaling pathway by which JAK3 differentially regulates TLR-mediated inflammatory cytokine production in innate immune cells.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1203084
Journal	The Journal of Immunology
Issue Number	3
Volume Number	191
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-08-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Glycogen Synthase Kinase 3 Metabolism Inflammation Immunology Janus Kinase 3 Toll-like Receptors Animals Cd4-positive T-lymphocytes Creb-binding Protein Cells, Cultured Dna-binding Proteins Antagonists & Inhibitors Immunity, Innate Genetics Interleukin-10 Biosynthesis Interleukin-17 Intestinal Mucosa Intestines Lipopolysaccharides Lymphocyte Activation Mice Monocytes Drug Effects Multiprotein Complexes Nf-kappa B Neutrophils Phosphatidylinositol 3-kinases Phosphorylation Proto-oncogene Proteins C-akt Rna Interference Rna, Small Interfering Signal Transduction Tor Serine-threonine Kinases Transcription Factor Rela Research Support, N.i.h., Extramural Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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