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. 2013 Sep 24;123(10):4364–4374. doi: 10.1172/JCI70064

Figure 1. Local IL-17A production is critical for wound healing.

Figure 1

(A) Il17a–/– mice have delayed wound closure in vivo. Wound-closure kinetics in WT, Tcrd–/–, and Il17a–/– mice were measured over time. Data shown represent percentage of wound area remaining open ± SEM from 4 to 8 wounds. **P ≤ 0.01; ***P ≤ 0.001, Il17a–/– versus WT. (B) Wound-healing kinetics were measured in SOCs from WT, Tcrd–/–, and Il17a–/– mice. In some conditions, wounded skin was supplemented with rIL-17A or vehicle control. Data are presented as mean ± SEM from 3 wounds per condition. *P ≤ 0.05; ***P ≤ 0.001, WT versus Il17a–/–. (C) Blockade of IL-17A inhibits wound closure in vivo. Neutralizing IL-17 Ab or control Ab (IgG2a) was applied into the wound bed of WT and Il17a–/– mice. Data are presented as the mean percentage of the wound area remaining open ± SEM from 4 to 8 wounds. *P ≤ 0.05; **P ≤ 0.01. (D) Recombinant IL-17A restores defective wound healing in Il17a–/– skin in vivo. Wounded skin was supplemented with rIL-17A or vehicle control, and wound-healing kinetics were measured over time. Data shown represent mean ± SEM of 4 to 8 wounds per condition. *P ≤ 0.05;**P ≤ 0.01; ***P ≤ 0.001, Il17a–/– versus WT.