2014
DOI: 10.1128/iai.00969-13
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MyD88- and TRIF-Independent Induction of Type I Interferon Drives Naive B Cell Accumulation but Not Loss of Lymph Node Architecture in Lyme Disease

Abstract: Rapidly after infection, live Borrelia burgdorferi, the causative agent of Lyme disease, is found within lymph nodes, causing rapid and strong tissue enlargement, a loss of demarcation between B cell follicles and T cell zones, and an unusually large accumulation of B cells. We sought to explore the mechanisms underlying these changes, as lymph tissue disruption could be detrimental for the development of robust Borrelia-specific immunity. A time course study demonstrated that the loss of the normal lymph node… Show more

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Cited by 38 publications
(39 citation statements)
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“…Consistent with this, in the mouse model of Lyme disease, CCL19 mRNA expression is increased in the lymph nodes of acutely infected mice (33). Elevated levels of CCL19 have also been observed during states of immune-mediated inflammation, including HIV infection, systemic lupus erythematosus, and rheumatoid arthritis (34)(35)(36)(37).…”
Section: Discussionsupporting
confidence: 60%
“…Consistent with this, in the mouse model of Lyme disease, CCL19 mRNA expression is increased in the lymph nodes of acutely infected mice (33). Elevated levels of CCL19 have also been observed during states of immune-mediated inflammation, including HIV infection, systemic lupus erythematosus, and rheumatoid arthritis (34)(35)(36)(37).…”
Section: Discussionsupporting
confidence: 60%
“…This culminates a decade of our work wherein two parallel pathways of investigation revealed a pathologic type I IFN profile in C3H mice infected with B. burgdorferi that is suppressed by IFNAR1 blockade (14, 1822). Others have corroborated the association between pathologic type I IFN production and Lyme disease pathogenesis in murine studies (52, 53) as well as in human patients at various stages of disease (2, 24), and many investigators have examined the type I IFN response to B. burgdorferi in murine and human cells (19, 20, 43, 5362). But the exact pathogenic member has remained elusive due to the transient expression of IFN-α/β (63, 64), overlapping interferon-stimulated gene pathways induced by IFN-α/β (65), and differing contexts of B. burgdorferi infection in which IFN-α/β transcripts have been detected.…”
Section: Discussionmentioning
confidence: 89%
“…Type I IFNs have also been identified in patients with various manifestations of Lyme disease, including skin lesions and cognitive deficits (63, 64), and have been implicated in B lymphocyte accumulation in the lymph nodes of infected mice (65). Taken in context with these previous findings, the current genetic identification of Bbaa1 implicates the cluster encoding the IFNαβ genes as a candidate regulator of Lyme arthritis.…”
Section: Discussionmentioning
confidence: 99%