Lymphocytes rapidly infiltrate into the brain following cardiac arrest and cardiopulmonary resuscitation (CA/CPR) (CAM5P.246)

• Published in: The Journal of immunology (1950) Vol. 192; no. 1_Supplement; pp. 180 - 180.17
• Main Authors: Carter, Jessica, Deng, Guiying, Wagner, David, Herson, Paco
• Format: Journal Article
• Language: English
• Published: 01.05.2014
• ISSN: 0022-1767; 1550-6606
• DOI: 10.4049/jimmunol.192.Supp.180.17

Abstract Isolated ischemic episodes, such as occurs with stroke, result in long-term neural damage. It is known that lymphocytes along with other immune cells infiltrate brain tissue promoting that process. During cardiac arrest, global ischemia then reperfusion occurs. Although inflammatory mechanisms have been linked to neuronal injury following global cerebral ischemia, the presence of infiltrating immune cells remains understudied. We examined the brains of mice at different time points after global cerebral ischemia induced by cardiac arrest and cardiopulmonary resuscitation (CA/CPR) and characterized the influx of lymphocytes into the injured brain. We observed that CA/CPR caused a rapid influx of lymphocytes within 3 hours of resuscitation that was maintained for the duration of our experiments. The large majority of infiltrating lymphocytes were CD4+ T cells that expressed the Th1 characteristic cytokines TNFα or INFγ. Of the CD4+ infiltrating cells, a large portion of them were also CD40+ (Th40). Brain injury models attribute much of the neural damage to microglia and subsequent oxidative stress. We found that the CA/CPR injury model was largely dependent upon T cells, and the lack of functional T cells in TCRα knockout mice significantly reduced neuronal injury. This data indicate that studies investigating the neuro-immune response after global cerebral ischemia should consider the role of infiltrating T cells in orchestrating the acute and sustained immune response.