Abstract:
:The symptoms of Lyme disease are caused by inflammation induced by species of the Borrelia burgdorferisensu lato complex. The various presentations of Lyme disease in the population suggest that differences exist in the intensity and regulation of the host response to the spirochete. Previous work has described correlations between the presence of regulatory T cells and recovery from Lyme arthritis. However, the effects of Foxp3-expressing CD4+ T cells existing prior to, and during, B. burgdorferi infection have not been well characterized. Here, we used C57BL/6 "depletion of regulatory T cell" mice to assess the effects these cells have on the arthritis-resistant phenotype characteristic of this mouse strain. We showed that depletion of regulatory T cells prior to infection with B. burgdorferi resulted in sustained swelling, as well as histopathological changes, of the tibiotarsal joints that were not observed in infected control mice. Additionally, in vitro stimulation of splenocytes from these regulatory T cell-depleted mice resulted in increases in gamma interferon and interleukin-17 production and decreases in interleukin-10 production that were not evident among splenocytes of infected mice in which Treg cells were not depleted. Depletion of regulatory T cells at various times after infection also induced rapid joint swelling. Collectively, these findings provide evidence that regulatory T cells existing at the time of, and possibly after, B. burgdorferi infection may play an important role in limiting the development of arthritis.
journal_name
Infect Immunjournal_title
Infection and immunityauthors
Siebers EM,Liedhegner ES,Lawlor MW,Schell RF,Nardelli DTdoi
10.1128/IAI.00160-20subject
Has Abstractpub_date
2020-10-19 00:00:00issue
11eissn
0019-9567issn
1098-5522pii
IAI.00160-20journal_volume
88pub_type
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