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. Author manuscript; available in PMC: 2015 Mar 17.
Published in final edited form as: Nat Med. 2014 Aug 17;20(9):1043–1049. doi: 10.1038/nm.3645

Figure 3.

Figure 3

Systemic JAK1/2 or JAK3 inhibition prevents the onset of AA in grafted C3H/HeJ mice. (a–j) AA development in C3H/HeJ grafted mice treated systemically from the time of grafting with ruxolitinib (JAK1/2i) (a,b) or tofacitinib (JAK3i) (f,g) (**P < 0.01). Frequency (number shown above boxed area) of CD8+NKG2D+ T cells in skin and cutaneous lymph nodes of mice treated with PBS or with JAK1/2i (c) or JAK3i (h) (***P < 0.001, statistical methods described in Supplementary Methods). Immunohistochemical staining of skin biopsies showing CD8 and MHC class I and II expression in skin of mice treated with PBS or with JAK1/2i (d) or JAK3i (i). ALADIN score of transcriptional analysis from mice treated with PBS or with JAK1/2i (e) or JAK3i (j), given as log2 mean expression Z-scores as indicated in the Supplementary Methods. Hair regrowth after an additional 12 weeks after treatment withdrawal is also shown. (a,f). Scale bars, 100 μm. For each experiment, n and number of repeats are detailed in the Supplementary Methods.