Firstly, Tregs can exert the anti-inflammatory effect by secretin

Firstly, Tregs can exert the anti-inflammatory effect by secreting the cytokine interleukin-10, which is widely acknowledged as anti-inflammatory cytokine (IL-10) [7]. The neuroprotective role of IL-10 was that noted decades DAPT secretase chemical structure ago for IL-10 could reduce brain injury following MCAO, whether administered intravenously or into lateral ventricle [29] and IL-10 knockout would result in enlarged infarcts [31]. In addition, Liesz et al. [55] confirmed the hypothesis in their Treg-depleted MCAO mouse model. On the basis of anti-CD25 mAb mediated Treg-depletion, exogenous IL-10 supplement would lead to a marked diminishment in infarct volume as compared with the controls.

Interestingly, it was also noticed that only intracerebroventricular injection, but not intraperitoneal injection, would result in the positive outcome, in consistency with the local accumulation of Tregs during the acute phase after stroke and suggested that the anti-inflammatory effect of IL-10 seems to be achieved by a direct action on brain cells [12]. Besides, Tregs conferred protection against MCAO by blunting a rise in metalloproteinases-9 (MMP-9) [51]. MMPs have been thought to be involved in stroke pathogenesis and clinical reports indicated elevated serum level of MMP-9 among patients with ischemic stroke [38]. Stroke-induced MMP-9 production owing to neutrophil infiltration played an important role during the breakdown of blood-brain barrier [39] and hence promoted leukocyte infiltration and brain damage [37], whereas Treg adoptive treatment inhibited MMP-9 production in the blood and the brain as early as 1 day after ischemia [51].

Tregs might exert this inhibitory capability via cell-to-cell contact with neutrophils as Tregs cultured into the transwells lost their inhibition on MMP9 production. 3.2.2. Cons In spite of all the positive contributions mentioned above, recent findings indicated a deleterious role of Tregs as well. As was shown in the experiment conducted by Kleinschnitz et al. [50], Tregs might exacerbate ischemic-reperfusion damage in a very early phase after stroke, that is, within 24 hours. This study accomplished Treg depletion via genetic modified mouse models, the DEREG mice, and in opposition to former discoveries, the authors found that, followed by 60min MCAO, Treg depletion should result in a decrease in infarct volume with an improvement in neurological function, and the beneficial effect would last out to 4 days; accordingly, MRI of depletion group showed smaller infarcts on day 1 without any evident progression observed throughout 1 week, which excluded the probability for a secondary growth.

Subsequently, the authors examined the influence of delayed Treg depletion. As a consequence, elimination of Tregs 1 day after 30min MCAO was not relevant to secondary growth Drug_discovery out to 1 week. Taken together, neither early nor delayed depletion was associated with a secondary growth in this study.

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