Ben D. Clarkson 

Ben D. Clarkson

Degree Program: Cellular and Molecular Pathology
Faculty Supervisor: Zsuzsanna Fabry
Phone: (608) 265-2982




Current Research

IL-21 in cerebral ischemia reperfusion injury. Several lines of evidence support deleterious roles for T cells that accumulate in post-ischemic organ tissues, such as liver, kidney, intestine and brain. It was proposed that T lymphocytes are detrimental in acute cerebral ischemic injuries as mice deficient in lymphocytes were protected from cerebral ischemia / reperfusion injury (cI/RI), and this protection could be abrogated by the adoptive transfer of CD4+ T cells. In spite of the critical importance of this observation, the T cell derived factors that enhance cerebral ischemic tissue injury are unknown. Preliminary results from our lab are the first to show that: (1) IL-21 cytokine is produced by perivascular cells in ischemic human brain tissue; (2) IL-21 in the post-ischemic mouse brain is predominantly produced by CD4+ T cells; (3) IL-21 deficient mice are protected from focal brain ischemia; (4) adoptive transfer of WT but not IL-21 KO CD4 T cells restores stroke injury in T-cell deficient mice; and (5) autophagy-related genes are upregulated in cells with neuronal morphology in ischemic brains from WT, but not IL-21 deficient mice. These data strongly implicate IL-21 in ischemic neuronal tissue damage. Manipulating IL-21 signaling with IL-21 antagonist might therefore be a novel therapeutic target for acute ischemic stroke.


Zozulya AL, Clarkson BD, Ortler S, Fabry Z, Wiendl H. The role of dendritic cells in CNS autoimmunity. J Mol Med (Berl) 2010, 88(6):535-44.

Clarkson BD, Héninger E, Harris MG, Lee J, Sandor M, Fabry Z. Innate-adaptive crosstalk: how dendritic cells shape immune responses in the CNS. Adv Exp Med Biol 2012;946:309-33.

Abstract (PDF)

Resume (PDF)





Biochemistry Department
433 Babcock Drive
Madison, WI 53706-1544

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