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. 2018 Mar;188(3):757–767. doi: 10.1016/j.ajpath.2017.11.012

Figure 4.

Figure 4

Depletion of γδT cells but not IL-17A/F or IL-22 protects the mouse brain from hypoxia-ischemia (HI)–induced preterm brain injury. A–H: γδT cell depletion as seen in the subcortical white matter volume by measuring the maltose-binding protein (MBP) immunohistochemical (IHC)–positive staining area (A, C, E, and F) and in the total tissue loss using microtubule associated protein (MAP)-2 IHC staining (B, D, G, and H) in Tcrd−/− and wild-type (WT) mice at 7 days after HI. A: Total volume of the subcortical white matter. B: Total brain tissue loss in the WT versus Tcrd−/− mouse brain. C and D: The total subcortical white matter area (C) and total brain tissue loss at the different brain levels (D). The x axis of C and B indicates the brain levels analyzed, where level 1 refers to the frontal part of the mouse brain and level 6 refers to the posterior part of the mouse brain. E–H: Representative images of the MBP (E and F) and MAP-2 (G and H) staining from the WT (E and G) and Tcrd−/− (F and H) mouse brains at 7 days after HI. I–L: Brain injury after blocking IL-17A/F or in Il22−/− mice at 7 days after HI. M and N: The Il17f and Il22 mRNA levels in WT, Tcrd−/−, and Rag1−/− mouse brains at 6 hours and 3 days after HI and in age-matched naïve control mice at postnatal day 5 (PND5) and postnatal day 8 (PND8), respectively. Data are expressed as means ± SEM (A–D, I–L) and as means ± SEM of the ratio of the target gene to the reference gene Gapdh (M and N). n = 29 Tcrd−/− and 29 WT mice at 7 days after HI (A–H); n = 20 IL-17, 19 anti–IL-17, 15 WT, and 20 Il22−/− mice (I–L); n = 7 to 10 control mice and 8 to 11 HI mice (M and N). P < 0.05, ∗∗P < 0.01, and ∗∗∗P < 0.001. TCR, T-cell receptor.