By Gregory W. Konat
The invention of toll-like receptors (TLRs) spurred the sector of innate immunity right into a renaissance after decades of forget. due to the fact that then, TLR learn has grown at an exponential expense. Taking an built-in methodological procedure, Signaling via Toll-Like Receptors deals a finished evaluation of significant suggestions in molecular biology, cellphone biology, biochemistry, genetics, and immunology and their serious software to the examine of toll-like receptor constitution, organic functionality, and the intracellular signaling caused via those receptors.
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The enigmatic plasmacytoid T cells develop into dendritic cells with interleukin (IL)-3 and CD40-ligand. J Exp Med 185, 1101, 1997. indb 20 5/9/08 5:06:33 PM Assessing the Response of Cells to TLR Stimulation 21 59. , Miller, J. , Anders, E. , Lahoud, M. , et al. Mouse plasmacytoid cells: long-lived cells, heterogeneous in surface phenotype and function, that differentiate into CD8(+) dendritic cells only after microbial stimulus. J Exp Med 196, 1307, 2002. 60. , and Trinchieri, G. Mouse type I IFN-producing cells are immature APCs with plasmacytoid morphology.
Triggering the interferon antiviral response through an IKK-related pathway. Science 300, 1148, 2003. 48. Fitzgerald, K. , McWhirter, S. , Faia, K. , Rowe, D. , Golenbock, D. , Coyle, A. , Liao, S. , and Maniatis, T. IKKepsilon and TBK1 are essential components of the IRF3 signaling pathway. Nat Immunol 4, 491, 2003. 49. McWhirter, S. , Fitzgerald, K. , Rowe, D. , Golenbock, D. , and Maniatis, T. IFN-regulatory factor 3-dependent gene expression is defective in Tbk1deficient mouse embryonic fibroblasts.
42 The physiological role of TRIF–TICAM-1 has been demonstrated by the generation of TRIF-mutant mice. 44 Thus, TRIF has been demonstrated to be essential for the TLR3- and TLR4mediated MyD88-independent pathway. 45,46 Thus, TRAM is essential for the TLR4-mediated MyD88-independent or TRIF-dependent pathway. In TRIF- and TRAM-deficient mice, inflammatory cytokine production induced by TLR2, TLR7, and TLR9 ligands is observed. 43,46 These findings indicate that TLR-mediated activation of the MyD88-dependent pathway is not impaired in these mice.
Signaling by Toll-Like Receptors by Gregory W. Konat