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. 2019 Sep 26;11(18):7402–7415. doi: 10.18632/aging.102239

Figure 6.

Figure 6

Treg cells mediate immune suppression in the spinal cord after SCI. (A) Mice were treated as in Figure 5A. ELISA analysis of cytokine concentration in the spinal cord at 7 days after sham or SCI surgery (n=5). (B, C) Mice were treated as in Figure 5B. (B) The cytokine concentration in the spinal cord at 7 days after sham or SCI surgery were determined as in (A) (n=5). (C) The proliferation rate of effector T cells was determined by [3H]-thymidine incorporation analysis (n=5). c.p.m., counts per minute of incorporated [3H]-thymidine. Data are mean ± SD. The statistical analysis was performed using Student’s t-test. **, P<0.01; *, P<0.05. (D) A brief schematic model of this study. After SCI, inflammatory cells infiltrate into the spinal cord and secrete cytokines, including IL-1β and TNF-α, which promptly induces the production of CCL28 via NF-κB activation. Responding to increased CCL28 in the focal sites, CCR10-expressing Treg cells are recruited and then exert their immune suppressive activities, restricting the inflammation to a controllable extent along with the time consumed. Owing to the activity of Treg cells recruited by CCL28, the local levels of IL-1β and TNF-α are decreased, thereby in turn relieving the stimulative effect on CCL28 upregulation, through this negative feed-back loop, CCL28 functions to suppress inflammation, reduce secondary damage and promotes locomotor recovery after SCI.