• Cristina Sastre, Matthew B Bevers, and W Taylor Kimberly.
• Center for Genomic Medicine and Department of Neurology, Massachusetts General Hospital, Lunder 644, 55 Fruit St, Boston, MA, 02114, USA.
• Neurocrit Care. 2021 Dec 1; 35 (3): 887893887-893.

AbstractFollowing both ischemic and hemorrhagic stroke, innate immune cells initiate a proinflammatory response that further exacerbate tissue injury in the acute phase, but these cells also play an important reparative role thereafter. Numerous cytokines and signaling pathways have been implicated in driving the deleterious proinflammatory response, but less is known about the mediators that connect the initial vascular injury to the systemic immune response and the relationship between proinflammatory and reparative immune responses. The Interleukin-33 (IL-33) and serum stimulation-2 (ST2) axis is an interleukin signaling pathway that is a prime candidate to fulfill this role. In this review, we describe the biology of the IL-33/ST2 system, present evidence that its soluble decoy receptor, soluble ST2 (sST2), plays a key role in secondary neurologic injury after stroke, and discuss this in the context of the known role of IL-33/ST2 in other disease.© 2021. Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society.

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