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Regulatory T Cells Contribute to Resistance against Lyme Arthritis
The symptoms of Lyme disease are caused by inflammation induced by species of the 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 betwe...
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Published in: | Infection and immunity 2020-10, Vol.88 (11) |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The symptoms of Lyme disease are caused by inflammation induced by species of the
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,
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
resulted in sustained swelling, as well as histopathological changes, of the tibiotarsal joints that were not observed in infected control mice. Additionally,
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,
infection may play an important role in limiting the development of arthritis. |
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ISSN: | 0019-9567 1098-5522 |
DOI: | 10.1128/IAI.00160-20 |