| First Author | Wan Y | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 5 | Pages | 3006-14 |
| PubMed ID | 21270393 | Mgi Jnum | J:169397 |
| Mgi Id | MGI:4940929 | Doi | 10.4049/jimmunol.1003217 |
| Citation | Wan Y, et al. (2011) The Dual Functions of IL-1 Receptor-Associated Kinase 2 in TLR9-Mediated IFN and Proinflammatory Cytokine Production. J Immunol 186(5):3006-14 |
| abstractText | Bone marrow-derived plasmacytoid dendritic cells (pDCs) from IL-1R-associated kinase (IRAK)2-deficient mice produced more IFNs than did wild-type pDCs upon stimulation with the TLR9 ligand CpG. Furthermore, in CpG-stimulated IRAK2-deficient pDCs there was increased nuclear translocation of IFN regulatory factor 7, the key transcription factor for IFN gene transcription in these cells. In IRAK2-deficient macrophages, enhanced NF-kappaB activation and increased expression of CpG-induced genes were detected within 2 h after treatment. However, at later times, NF-kappaB activation was decreased and, in contrast to the results with IFN, there was less secretion of other proinflammatory cytokines (such as TNF-alpha) and chemokines in CpG-stimulated IRAK2-deficient pDCs and macrophages. Therefore, although IRAK2 is a negative regulator of TLR9-mediated IFN production through its modulation of the transcriptional activity of IFN regulatory factor 7, it is also a positive regulator of TLR9-mediated proinflammatory cytokine and chemokine production at some level subsequent to transcription. |
