| First Author | Clarkson BD | Year | 2014 |
| Journal | J Exp Med | Volume | 211 |
| Issue | 4 | Pages | 595-604 |
| PubMed ID | 24616379 | Mgi Jnum | J:210825 |
| Mgi Id | MGI:5571952 | Doi | 10.1084/jem.20131377 |
| Citation | Clarkson BD, et al. (2014) T cell-derived interleukin (IL)-21 promotes brain injury following stroke in mice. J Exp Med 211(4):595-604 |
| abstractText | 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. |
