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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Jain, Aakanksha Dozmorov, Igor M. Hu, Wei Gao, Yajing Mandraju, Rajakumar Pasare, Chandrashekhar Wakeland, Edward K. |
| Description | Author Affiliation: Hu W ( Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9093.); Jain A ( Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9093.); Gao Y ( Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9093.); Dozmorov IM ( Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9093.); Mandraju R ( Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9093.); Wakeland EK ( Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9093.); Pasare C ( Department of Immunology, University of Texas Southwestern Medical Center, Dallas, TX 75390-9093 chandrashekhar.pasare@utsouthwestern.edu.); |
| Abstract | Recognition of pathogen-associated molecular patterns by Toll-like receptors (TLRs) on dendritic cells (DCs) leads to DC maturation, a process involving up-regulation of MHC and costimulatory molecules and secretion of proinflammatory cytokines. All TLRs except TLR3 achieve these outcomes by using the signaling adaptor myeloid differentiation factor 88. TLR4 and TLR3 can both use the Toll-IL-1 receptor domain-containing adaptor inducing IFN-ß (TRIF)-dependent signaling pathway leading to IFN regulatory factor 3 (IRF3) activation and induction of IFN-ß and - 4. The TRIF signaling pathway, downstream of both of these TLRs, also leads to DC maturation, and it has been proposed that the type I IFNs act in cis to induce DC maturation and subsequent effects on adaptive immunity. The present study was designed to understand the molecular mechanisms of TRIF-mediated DC maturation. We have discovered that TLR4-TRIF-induced DC maturation was independent of both IRF3 and type I IFNs. In contrast, TLR3-mediated DC maturation was completely dependent on type I IFN feedback. We found that differential activation of mitogen-activated protein kinases by the TLR4- and TLR3-TRIF axes determined the type I IFN dependency for DC maturation. In addition, we found that the adjuvanticity of LPS to induce T-cell activation is completely independent of type I IFNs. The important distinction between the TRIF-mediated signaling pathways of TLR4 and TLR3 discovered here could have a major impact in the design of future adjuvants that target this pathway. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 45 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-11-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Adaptor Proteins, Vesicular Transport Metabolism Dendritic Cells Immunology Gene Expression Regulation Signal Transduction Physiology Toll-Like Receptor 3 Toll-Like Receptor 4 Animals Blotting, Western CD4-Positive T-Lymphocytes Cell Proliferation Cytology Flow Cytometry Lipopolysaccharides Mice Mice, Knockout Molecular Sequence Data Sequence Analysis, RNA Research Support, N.I.H., Extramural Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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