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Endothelial cells and fibroblasts amplify the arthritogenic type I IFN response in murine Lyme disease and are major sources of chemokines in Borrelia burgdorferi-infected joint tissue. | LitMetric

AI Article Synopsis

  • - The study investigates severe Lyme arthritis in C3H mice infected with Borrelia burgdorferi, focusing on the role of type I interferon (IFN) and how it contributes to the disease process.
  • - Researchers used genetically modified mice lacking the type I IFN receptor to analyze how various joint cells contribute to the IFN response, revealing that myeloid cells, endothelial cells, and fibroblasts played key roles.
  • - The findings highlight complex interactions between different cell types in the joint that trigger the IFN response, suggesting similar mechanisms could be relevant for other diseases linked to type I IFN, like lupus and certain rheumatoid arthritis forms.

Article Abstract

Localized elevation in type I IFN has been uniquely linked to the severe Lyme arthritis that develops in C3H mice infected with the spirochete Borrelia burgdorferi. In this study, the dynamic interactions that result in generation of these responses were further examined in C3H mice carrying the type I IFN receptor gene ablation, which effectively blocks all autocrine/paracrine signaling crucial to induction of downstream effectors. Reciprocal radiation chimeras between C3H and IFNAR1⁻/⁻ mice implicated both radiation-sensitive and radiation-resistant cells of the joint tissue in the proarthritic induction of type I IFN. Ex vivo analysis of cells from the naive joint revealed CD45⁺ cells residing in the tissue to be uniquely capable of initiating the type I IFN response to B. burgdorferi. Type I IFN responses were analyzed in real time by lineage sorting of cells from infected joint tissue. This demonstrated that myeloid cells, endothelial cells, and fibroblasts were responsible for propagating the robust IFN response, which peaked at day 7 postinfection and rapidly resolved. Endothelial cells and fibroblasts were the dominant sources of IFN signature transcripts in the joint tissue. Fibroblasts were also the major early source of chemokines associated with polymorphonuclear leukocyte and monocyte/macrophage infiltration, thus providing a focal point for arthritis development. These findings suggest joint-localized interactions among related and unrelated stromal, endothelial, and myeloid cell lineages that may be broadly applicable to understanding the pathogeneses of diseases associated with type I IFN signature, including systemic lupus erythematosus and some rheumatoid arthritides.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3424307PMC
http://dx.doi.org/10.4049/jimmunol.1201095DOI Listing

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