| First Author | Bhattacharyya S | Year | 2010 |
| Journal | Blood | Volume | 115 |
| Issue | 10 | Pages | 1921-31 |
| PubMed ID | 20065289 | Mgi Jnum | J:158841 |
| Mgi Id | MGI:4440706 | Doi | 10.1182/blood-2009-06-224782 |
| Citation | Bhattacharyya S, et al. (2010) TAK1 targeting by glucocorticoids determines JNK and IkappaB regulation in Toll-like receptor-stimulated macrophages. Blood 115(10):1921-31 |
| abstractText | 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 kappaB (IkappaB) degradation or Janus kinase (JNK) activation. Moreover, the sensitivity of transforming growth factor beta-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. |
