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Open AccessJournal ArticleDOI

The immunology of stroke: from mechanisms to translation

Costantino Iadecola, +1 more
- 01 Jul 2011 - 
- Vol. 17, Iss: 7, pp 796-808
TLDR
Gaining a better understanding of the reciprocal interaction between the immune system and the ischemic brain is essential to harness the full therapeutic potential of the immunology of stroke.
Abstract
Immunity and inflammation are key elements of the pathobiology of stroke, a devastating illness second only to cardiac ischemia as a cause of death worldwide. The immune system participates in the brain damage produced by ischemia, and the damaged brain, in turn, exerts an immunosuppressive effect that promotes fatal infections that threaten the survival of people after stroke. Inflammatory signaling is involved in all stages of the ischemic cascade, from the early damaging events triggered by arterial occlusion to the late regenerative processes underlying post-ischemic tissue repair. Recent developments have revealed that stroke engages both innate and adaptive immunity. But adaptive immunity triggered by newly exposed brain antigens does not have an impact on the acute phase of the damage. Nevertheless, modulation of adaptive immunity exerts a remarkable protective effect on the ischemic brain and offers the prospect of new stroke therapies. As immunomodulation is not devoid of deleterious side effects, a better understanding of the reciprocal interaction between the immune system and the ischemic brain is essential to harness the full therapeutic potential of the immunology of stroke.

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Neuroinflammation: friend and foe for ischemic stroke

TL;DR: How neuroinflammation has both beneficial as well as detrimental roles and recent therapeutic strategies to combat pathological responses are discussed and the time-dependent role of inflammatory factors could help in developing new diagnostic, prognostic, and therapeutic neuroprotective strategies for post-stroke inflammation.
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Commensal microbiota affects ischemic stroke outcome by regulating intestinal γδ T cells.

TL;DR: It is shown that antibiotic-induced alterations in the intestinal flora reduce ischemic brain injury in mice, an effect transmissible by fecal transplants, and that IL-10 and IL-17 are required for the neuroprotection afforded by intestinal dysbiosis.
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