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English: F2: IL-6 has a major role in the response of the brain to injury. To some extent the response of the brain to trauma and stroke is similar. Stroke may be caused by an embolus/thrombus occlusion, an hemorrhage or a vasospasm, resulting in ischemia. Hypoxia initiates a biochemical cascade leading towards cell death, involving excitotoxicity, oxidative stress and apoptosis in which IL-6 has a protective effect. In the early response, neutrophils extravasate to nervous parenchyma involving a process of rolling, activation and transmigration due to an upregulation of P and E-selectin, followed then by an upregulation of ICAM and VCAM. Neutrophils are a rich source of sIL-6R, and damaged resident cells produce IL-6, TNF-α, IL-1β and chemokines, enhancing leukocyte migration toward parenchyma. TNF-α and IL-1β lead to neutrophil degranulation and tissue destruction by means of metalloproteinase (MMP) and TGF-β, while IL-6 inhibits TNF-α and neutrophils' diapedesis. Moreover, it induces apoptosis in neutrophils in a negative feedback loop. In the late phase of this response, IL-6 orchestrates the transition between innate and adaptive immune response, not only inhibiting neutrophils but recruiting monocytes and T-cells for a late inflammatory response. Besides, it induces astrogliosis and angiogenesis needed for the tissue remodelation and recovering. On the other hand, IL-6 exhibits a detrimental effect for instance in relation with body temperature increase, critical in the patient outcome. If deregulated, chronic IL-6 may cause significant brain damage.