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Figures

Figure 1

JAK inhibition leads to improvement in patients with morphea and prevents bleomycin-induced fibrosis in mice. a, Patients treated with baricitinib (lower left) or tofacitinib. b, Gross, H&E, and trichrome (Tri) stained sections, scale bar: 50 μM. c, Morphea severity scores *Indicates that 2 patients had identical scores. d, Phospho-STAT1/3 staining in morphea, scale bar: 25 μM. e, Skin thickness (mean+/-SEM) in bleomycin-treated mice, V: vehicle, T: tofacitinib, R: ruxolitinib. f, Normal (Cont) and bleomycin-treated murine skin stained with phospho-STAT3, scale bar: 25 μM. g, Quantification of d. h, COL1A1 expression in human fibroblasts treated with bleomycin +/- JAK inhibitors (10 μM), normalized to HPRT1 expression. Dotted line: baseline COL1A1. ***p = 0.004 (vs Veh), **p = 0.038 (vs Veh). i, Quantification of f. j, Col1a1 expression (mean+/-SEM) in skin from bleomycin-treated mice; normalized to Actb. *p=0.07 vs Veh (V), **p=0.11 vs Veh, ***, p=0.04 vs Veh. All patients consented to publication of their clinical images.

Figure S1

Patient #2 had recurrence worsening of morphea and recurrence of ulcerative lesions after discontinuation of tofacitinb.

Figure S2

Sex-specific effects of bleomycin and JAKi treatment in mice. ++Two outlier values are outside the axis of the data displayed for male vehicle (87.2 and 51.7).

To the Editor, Morphea is an autoimmune disease that causes fibrosis of the skin that may result in significant morbidity. Eosinophilic fasciitis (EF) may be considered a deeper form of morphea, and features of both morphea and EF can be present in individual patients. Morphea and EF have been postulated to have pathogenic features that overlap with systemic sclerosis (Laxer and Zulian, 2006). In these diseases, dysregulated immune responses are thought to induce fibrosis (Torok et al., 2019). Treatment of these diseases with non-specific immunosuppressants such as corticosteroids is often ineffective and associated with toxicity.

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