TLR2 modulates inflammation in zymosan-induced arthritis in mice |
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Authors: | Matthias?E?Frasnelli David?Tarussio Veronique?Chobaz-Péclat Nathalie?Busso Email author" target="_blank">Alexander?SoEmail author |
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Institution: | (1) Laboratoire de Rhumatologie, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland |
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Abstract: | The interplay between the innate and acquired immune systems in chronic inflammation is not well documented. We have investigated
the mechanisms of inflammation in murine zymosan-induced arthritis (ZIA) in the light of recent data on the roles of Toll-like
receptor 2 (TLR2) and Dectin-1 in the activation of monocyte/macrophages by zymosan. The severity of inflammation, joint histology,
lymphocyte proliferation and antibody production in response to zymosan were analyzed in mice deficient in TLR2 and complement
C3, and the effects of Dectin-1 inhibition by laminarin were studied. In comparison with wild-type animals, TLR2-deficient
mice showed a significant decrease in the early (day 1) and late phases (day 24) of joint inflammation. C3-deficient mice
showed no differences in technetium uptake or histological scoring. TLR2-deficient mice also showed a significant decrease
in lymph node cell proliferation in response to zymosan and a lower IgG antibody response to zymosan at day 25 in comparison
with wild-type controls, indicating that TLR2 signalling has a role in the development of acquired immune responses to zymosan.
Although laminarin, a soluble β-glucan, was able to significantly inhibit zymosan uptake by macrophages in vitro, it had no effect on ZIA in vivo. These results show that ZIA is more prolonged than was originally described and involves both the innate and acquired immune
pathways. C3 does not seem to have a major role in this model of joint inflammation. |
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