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. Author manuscript; available in PMC: 2020 Apr 1.
Published in final edited form as: J Allergy Clin Immunol. 2018 Sep 19;143(4):1426–1443.e6. doi: 10.1016/j.jaci.2018.08.042

Figure 2. Skin inflammation is dependent on MyD88 signaling.

Figure 2.

Skin injury was performed on ft/ft and ft/ft × MyD88−/− mice. (A) Representative digital photographs on day 21. (B) Representative histology (H&E) from day 21 (scale bars = 200 μm). (C) Mean area of skin inflammation cm2 ± s.e.m. (D) Mean epidermal thickness (μm) ± s.e.m. (E) Mean number ± s.e.m. of PMNs, monocytes and eosinophils per million cells from day 21 skin. (F) Representative digital photographs on day 21 of ft/ft mice treated with Vehicle (sterile water) or FTY720. (G) Representative histology (H&E) from day 21 (scale bars = 200 μm). (H) Mean area of skin inflammation cm2 ± s.e.m. (I) Mean epidermal thickness (μm) ± s.e.m. (J) Mean number ± s.e.m. of PMNs, monocytes and eosinophils per million cells from day 21 skin. (K) Mean number of unstimulated CD4+ and γδ T cells per million cells ± s.e.m. from day 21 skin of ft/ft mice treated with PBS or FTY720. *P<0.05, †P<0.01, ‡P<0.001, ft/ft vs. ft/ft × MyD88−/− mice or Vehicle vs. FTY720, as calculated by two-tailed Student’s t-test. Results are representative of 2 independent experiments (n = 3–5 mice/group per experiment).