NDLI: TAK1 targeting by glucocorticoids determines JNK and IκB regulation in Toll-like receptor

Content Provider	PubMed Central
Author	Bhattacharyya, Sandip Ratajczak, Christine K. Vogt, Sherri K. Kelley, Crystal Colonna, Marco Schreiber, Robert D. Muglia, Louis J.
Abstract	Glucocorticoids potently attenuate the production of inflammatory mediators by macrophages, a primary effector of innate immunity. Activation of different macrophage Toll-like receptors (TLRs) by their respective ligands presents a powerful system by which to evaluate stimulus-dependent glucocorticoid effects in the same cell type. Here, we test the hypothesis that glucocorticoids, acting through the glucocorticoid receptor, modulate macrophage activation preferentially depending upon the TLR-selective ligand and TLR adapters. We established that 2 adapters, Trif, MyD88, or both, determine the ability of glucocorticoids to suppress inhibitor of κB (IκB) degradation or Janus kinase (JNK) activation. Moreover, the sensitivity of transforming growth factor β–activated kinase 1 (TAK1) activation to glucocorticoids determines these effects. These findings identify TAK1 as a novel target for glucocorticoids that integrates their anti-inflammatory action in innate immunity signaling pathways.
Related Links	http://dx.doi.org/10.1182/blood-2009-06-224782
Ending Page	1931
Page Count	11
Starting Page	1921
File Format	PDF
ISSN	00064971
e-ISSN	15280020
Journal	Blood
Issue Number	10
Volume Number	115
Language	English
Publisher	American Society of Hematology
Publisher Date	2010-03-11
Access Restriction	Open
Rights Holder	American Society of Hematology
Subject Keyword	Immunology Cell Biology Biochemistry Hematology Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Cell Biology Hematology Biochemistry Immunology

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4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
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