γδ T cells provide the early source of IFN-γ to aggravate lesions in spinal cord injury.
Guodong SunShuxian YangGuangchao CaoQianghua WangJianlei HaoQiong WenZhizhong LiKwok-Fai SoZonghua LiuSufang ZhouYongxiang ZhaoHengwen YangLibing ZhouZhinan YinPublished in: The Journal of experimental medicine (2017)
Immune responses and neuroinflammation are critically involved in spinal cord injury (SCI). γδ T cells, a small subset of T cells, regulate the inflammation process in many diseases, yet their function in SCI is still poorly understood. In this paper, we demonstrate that mice deficient in γδ T cells (TCRδ-/- ) showed improved functional recovery after SCI. γδ T cells are detected at the lesion sites within 24 hours after injury and are predominantly of the Vγ4 subtype and express the inflammatory cytokine IFN-γ. Inactivating IFN-γ signaling in macrophages results in a significantly reduced production of proinflammatory cytokines in the cerebrospinal fluid (CSF) of mice with SCIs and improves functional recovery. Furthermore, treatment of SCI with anti-Vγ4 antibodies has a beneficial effect, similar to that obtained with anti-TNF-α. In SCI patients, γδ T cells are detected in the CSF, and most of them are IFN-γ positive. In conclusion, manipulation of γδ T cell functions may be a potential approach for future SCI treatment.
Keyphrases
- spinal cord injury
- immune response
- spinal cord
- dendritic cells
- neuropathic pain
- cerebrospinal fluid
- oxidative stress
- end stage renal disease
- ejection fraction
- newly diagnosed
- rheumatoid arthritis
- type diabetes
- peritoneal dialysis
- high fat diet induced
- cognitive impairment
- metabolic syndrome
- inflammatory response
- prognostic factors
- combination therapy
- lipopolysaccharide induced
- risk assessment
- wild type
- patient reported outcomes
- climate change
- skeletal muscle
- brain injury
- smoking cessation