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. Author manuscript; available in PMC: 2009 Aug 1.
Published in final edited form as: Exp Mol Pathol. 2008 Apr 8;85(1):20–27. doi: 10.1016/j.yexmp.2008.03.004

Fig. 7. In the absence of TLR2 the IFNβ response is unchecked, resulting in exaggerated arthritis.

Fig. 7

In wild-type animals, B. burgdorferi lipoproteins signal through TLR2, resulting in downstream activation of NF-kB and production of pro-inflammatory and anti-inflammatory cytokines. The presence of anti-inflammatory cytokines (i.e. IL-10) blocks the feedback amplification of Type I IFN, which is present due to PAMP receptor-mediated signaling events. In TLR2−/− mice, the lack of TLR2 signaling prevents cytokine production, resulting in uninhibited amplification of the Type I IFN response and the development of severe arthritis.