Genetic Control of Lyme Arthritis by Borrelia burgdorferi Arthritis–Associated Locus 1 Is Dependent on Localized Differential Production of IFN-β and Requires Upregulation of Myostatin

作者： Jackie K. Paquette , Ying Ma , Colleen Fisher , Jinze Li , Sang Beum Lee

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摘要: Previously, using a forward genetic approach, we identified differential expression of type I IFN as positional candidate for an quantitative trait locus underlying Borrelia burgdorferi arthritis-associated 1 (Bbaa1). In this study, show that mAb blockade revealed unique role IFN-β in Lyme arthritis development B6.C3-Bbaa1 mice. Genetic control was also bone marrow-derived macrophages stimulated with B. burgdorferi, and it responsible feed-forward amplification IFN-stimulated genes. Reciprocal radiation chimeras between C57BL/6 mice is initiated by radiation-sensitive cells, but orchestrated radiation-resistant components joint tissue. Advanced congenic lines were developed to reduce the physical size Bbaa1 interval, confirmed contribution genes arthritis. RNA sequencing resident CD45- cells from advanced interval-specific recombinant myostatin uniquely upregulated association development, linked production. Inhibition vivo suppressed reduced interval mice, formally implicating novel downstream mediator joint-specific inflammatory response burgdorferi.

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Genetic Control of Lyme Arthritis by Borrelia burgdorferi Arthritis–Associated Locus 1 Is Dependent on Localized Differential Production of IFN-β and Requires Upregulation of Myostatin

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Genetic Control of Lyme Arthritis by Borrelia burgdorferi Arthritis–Associated Locus 1 Is Dependent on Localized Differential Production of IFN-β and Requires Upregulation of Myostatin

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