TLR9 triggers MyD88-independent anti-inflammatory signaling in lupus |
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| Affiliation: | 1. Department of Immunology, Institute of Basic Medical Sciences, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China;2. Institute of Immunology, College of Life Sciences, Nankai University, Tianjin, China;1. Division of Human Nutrition and Health, Wageningen University, Wageningen, The Netherlands;2. Department of Internal Medicine, RadboudUMC, Nijmegen, The Netherlands;1. Department of Immunology, St. Jude Children''s Research Hospital, Memphis, TN, 38105, USA;1. The Walter and Eliza Hall Institute of Medical Research, Parkville, Melbourne, VIC 3052, Australia;2. Department of Medical Biology, The University of Melbourne, Melbourne, VIC 3010, Australia;3. The University of Queensland Frazer Institute, Faculty of Medicine, The University of Queensland, Brisbane, QLD 4102, Australia;1. Department of Immunology, St. Jude Children''s Research Hospital, Memphis, TN 38105, USA;1. Department of Biotechnological and Applied Clinical Sciences (DISCAB), University of L’Aquila, 67100 L’Aquila, Italy;2. Department of Immunology and Inflammation, Imperial College London, London W12 0NN, UK |
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| Abstract: | Activation of Toll-like receptor 7 (TLR7) can induce lupus in mice, whereas activation of TLR9 can prevent it, even though both receptors interact with myeloid differentiation primary response gene 88 (MyD88) for downstream signaling. How TLR9 triggers anti-inflammatory responses in autoimmunity is unclear. Leibler et al. recently reported that TLR9 initiates anti-inflammatory signaling and inhibits lupus pathogenesis in a MyD88-independent but ligand-dependent manner. |
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