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. Author manuscript; available in PMC: 2011 May 3.
Published in final edited form as: J Invest Dermatol. 2010 Jul 8;130(11):2583–2593. doi: 10.1038/jid.2010.200

Figure 3. Induction of TGFβ-responsive genes by TLR ligands in SSc and normal dermal fibroblasts.

Figure 3

(a) Increased COMP mRNA expression in dcSSc and LE skin compared to control skin. (b and c) COMP and PAI-1 mRNA expression by dermal fibroblasts from dcSSc ( Inline graphic) and control (△) subjects treated with TLR agonists (as in Fig. 1), IFN α/β, IFNγ or TGFβ. (b and c) COMP and PAI-1 expression show significant induction with agonists of TLR2 (p<0.05), TLR3/Poly(I:C) (p<0.05), and TGFβ, (p<0.001). (d) mRNA expression of TLR3 mRNA expression in lesional (SSc L; 1.5-fold increase, p=ns), in non-lesional skin (SSc N/L; 0.92-fold increase, p=ns) from dcSSc patients compared to control skin (n=6). (e) Increased TLR3 mRNA expression by dermal fibroblasts from control (△) and dcSSc ( Inline graphic) subjects cultured as in Fig. 2: TLR2 agonist (17.1 fold-increase, p<0.05); TLR3 agonist (86.9 fold-increase, p<0.00001); IFNα (56.1 fold-increase, p<0.00001); IFNβ (39.5 fold-increase, p<0.00001); and IFNγ (13.8 fold-increase, p<0.01). (f) Immunohistochemical staining with anti-TLR3 (left panel) and control Ig (right panel) in dcSSc skin.