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CD8 T cell-derived perforin aggravates secondary spinal cord injury through destroying the blood-spinal cord barrier

Zhaoxiang Liu, Hua Zhang, Hong Xia, Baocheng Wang, Renwen Zhang, Qun Zeng, Lingzhi Guo, Kui Shen, BaTa Wang, Yanheng Zhong, Zhizhong Li, Guodong Sun
Biochemical and biophysical research communications 2019 v.512 no.2 pp. 367-372
CD8-positive T-lymphocytes, animal injuries, animal models, biotin, cerebrospinal fluid, cytokines, enzyme-linked immunosorbent assay, flow cytometry, humans, infectious diseases, inflammation, mice, permeability, spinal cord, staining
Perforin plays an important role in autoimmune and infectious diseases, but its function in immune inflammatory responses after spinal cord injury (SCI) has received insufficient attention. The goal of this study is to determine the influence of perforin after spinal cord injury (SCI) on secondary inflammation. Compared recovery from SCI in perforin knockout (Prf1−/−) and wild-type(WT)mice, WT mice had significantly lower the Basso mouse score (BMS), CatWalk XT, and motor-evoked potentials (MEPs) than Prf1−/− mice. Spinal cord lesions were also more obvious through glial fibrillary acidic protein (GFAP), Nissl, and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) staining. Furthermore, the blood-spinal cord barrier (BSCB) disruption was more severe and inflammatory cytokine levels were higher. Flow cytometry indicated that perforin mainly originated from CD8 T cells. With flow cytometry and enzyme-linked immunosorbent assay (ELISA), human cerebrospinal fluid (CSF) yielded similar results. Together, this study firstly demonstrated that CD8 T cell-derived perforin is detrimental to SCI recovery in the mouse model. Mechanistically, this effect occurs because perforin increases BSCB permeability, causing inflammatory cells and related cytokines to infiltrate and disrupt the nervous system.