T cell–derived interleukin (IL)-21 promotes brain injury following stroke in mice
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Author
Clarkson, Benjamin D.S.
Ling, Changying
Shi, Yejie
Harris, Melissa G.
Rayasam, Aditya
Sun, Dandan
Salamat, M. Shahriar
Lambris, John D.
Sandor, Matyas
Fabry, Zsuzsanna
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1084/jem.20131377Metadata
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Clarkson, B. D., C. Ling, Y. Shi, M. G. Harris, A. Rayasam, D. Sun, M. S. Salamat, et al. 2014. “T cell–derived interleukin (IL)-21 promotes brain injury following stroke in mice.” The Journal of Experimental Medicine 211 (4): 595-604. doi:10.1084/jem.20131377. http://dx.doi.org/10.1084/jem.20131377.Abstract
T lymphocytes are key contributors to the acute phase of cerebral ischemia reperfusion injury, but the relevant T cell–derived mediators of tissue injury remain unknown. Using a mouse model of transient focal brain ischemia, we report that IL-21 is highly up-regulated in the injured mouse brain after cerebral ischemia. IL-21–deficient mice have smaller infarcts, improved neurological function, and reduced lymphocyte accumulation in the brain within 24 h of reperfusion. Intracellular cytokine staining and adoptive transfer experiments revealed that brain-infiltrating CD4+ T cells are the predominant IL-21 source. Mice treated with decoy IL-21 receptor Fc fusion protein are protected from reperfusion injury. In postmortem human brain tissue, IL-21 localized to perivascular CD4+ T cells in the area surrounding acute stroke lesions, suggesting that IL-21–mediated brain injury may be relevant to human stroke.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3978271/pdf/Terms of Use
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