Fig. 2.

The absence of NK cells does not have a major effect on muscle regeneration or fibrosis development. (A) Picrosirius red and nuclei staining of TA muscle sections from damaged control (isotype treated) and NK-depleted WT mice. (B) Distribution of centrally nucleated myofiber cross sectional area (CSA) of damaged muscles from control and NK-depleted WT mice (n = 5 mice per group, Brown–Forsythe and Welch ANOVA tests followed by Dunnett’s T3 multiple comparisons test on selected bins). (C) Distribution of centrally nucleated myofiber CSA of damaged muscles from NOD SCID and NSG mice (n = 4 mice per group, Brown–Forsythe and Welch ANOVA tests followed by Dunnett’s T3 multiple comparisons test on selected bins). (D) Picrosirius red and nuclei staining of diaphragm sections from control (isotype treated) and NK-depleted Dmd^mdx mice. (E) Distribution of myofiber CSA from control and NK-depleted Dmd^mdx mice (n = 5 mice for control and n = 6 mice for NK-depleted Dmd^mdx, Brown–Forsythe and Welch ANOVA tests followed by Dunnet’s T3 multiple comparisons test on selected bins). (F) Ex vivo functional analysis of dystrophic diaphragm muscle from control and NK-depleted Dmd^mdx mice (each dot represents one mouse, unpaired t test).