Increased frequency of circulating regulatory T cells in patients with acute cerebral hemorrhage

Shi, Lei; Qin, Jie; Song, Bo; Wang, Qing Mei; Zhang, Rui; Liu, Xinjing; Liu, Yutao; Hou, Haiman; Chen, Xiu-Lan; Ma, Xiaobo; Jiang, Chenyang; Sun, Xiao Fei; Gong, Guangming; Xu, Yuming

doi:10.1016/j.neulet.2015.02.042

Cited by 21 publications

(19 citation statements)

References 25 publications

(51 reference statements)

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“…Previous reports are conflicting in regard to the effect of stroke on the frequency or percentage of Treg cells [7, 22–24]. Similar to our previous findings in an animal model [22], we found that the percentage of Treg cells in the lymphocyte population increased, whereas the percentages of Th cells, cytotoxic T cells, NK cells, and B lymphocytes all significantly decreased during the early phase after ischemic stroke.…”

Section: Discussionsupporting

confidence: 88%

Changes in the cellular immune system and circulating inflammatory markers of stroke patients

et al. 2016

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This study was designed to investigate dynamic changes in the cellular immune system and circulating inflammatory markers after ischemic stroke. Blood was collected from 96 patients and 99 age-matched control subjects for detection of lymphocyte subpopulations and inflammatory markers. We observed decreases in B cells, Th cells, cytotoxic T cells, and NK cells and an increase in regulatory T (Treg) cells in stroke patients on days 1, 3, and 7. Serum levels of TNF-a, C-reactive protein (CRP), IL-4, IL-6, IL-10, IL-17, IL-23, and TGF-β increased, whereas serum level of IFN-? decreased at all time points after stroke. Stroke patients with infection exhibited a similar tendency toward changes in some lymphocyte subpopulations and inflammatory markers as stroke patients without infection. After controlling for NIH Stroke Scale (NIHSS), we observed no differences in lymphocyte subpopulations between patients with anterior circulation stroke and those with posterior circulation stroke at any time point. The splenic volume correlated positively with the percentages of B cells, Th cells, and cytotoxic T cells, but negatively with Treg cells on day 3 after stroke. Infections were associated with splenic volume, leukocyte counts, percentage of Treg cells, and serum levels of CRP, IL-10, and IFN-? on day 3. Lesion volume correlated positively with CRP, IL-6, and IL-23, but negatively with IFN-? on day 3. The NIHSS showed a positive relation with IL-6 and IL-10 on day 3. Ischemic stroke has a profound effect on the systemic immune system that might explain the increased susceptibility of stroke patients to infection.

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Section: Discussionsupporting

confidence: 88%

Changes in the cellular immune system and circulating inflammatory markers of stroke patients

et al. 2016

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“…IL-10 also induces production of suppressor of cytokine signalling (SOCS)1 and SOCS3, which suppress pro-inflammatory cytokine production via signal transducer and activator of transcription (STAT)3 in macrophages 86,87 . Interestingly, IL-10 levels in blood 88–90 and brain tissue 90,91 are increased in patients with ICH, as well as in preclinical models of ICH 50,92,93 . IL-10 levels are increased in patients during the early acute phase of spontaneous ICH, and this rise is associated with subsequent rebleeding 89 , although this relationship is not necessarily causal.…”

Section: Microgliamentioning

confidence: 99%

“…In patients with ICH, the frequency of both activated (CD3 + CD9 + ) and regulatory (CD4 + CD25 + FOXP3 + ) T cells (T reg cells) 166,167 was increased in the peripheral blood of patients from day 3 to day 7 after ICH 90 . In mice with blood-induced ICH, T reg cells 45 and γδ T cells 168 infiltrated the brain starting at day 4, and their levels remained elevated until day 7; furthermore, these T reg cells inhibited M1 microglia in vitro 169 and in vivo 170 .…”

Section: Microglial Interactions With Other Cellsmentioning

confidence: 99%

Modulators of microglial activation and polarization after intracerebral haemorrhage

et al. 2017

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Intracerebral haemorrhage (ICH) is the most lethal subtype of stroke but currently lacks effective treatment. Microglia are among the first non-neuronal cells on the scene during the innate immune response to ICH. Microglia respond to acute brain injury by becoming activated and developing classic M1-like (proinflammatory) or alternative M2-like (anti-inflammatory) phenotypes. This polarization implies as yet unrecognized actions of microglia in ICH pathology and recovery, perhaps involving microglial production of proinflammatory or anti-inflammatory cytokines and chemokines. Furthermore, alternatively activated M2-like microglia might promote phagocytosis of red blood cells and tissue debris, a major contribution to haematoma clearance. Interactions between microglia and other cells modulate microglial activation and function, and are also important in ICH pathology. This Review summarizes key studies on modulators of microglial activation and polarization after ICH, including M1-like and M2-like microglial phenotype markers, transcription factors and key signalling pathways. Microglial phagocytosis, haematoma resolution, and the potential crosstalk between microglia and T lymphocytes, neurons, astrocytes, and oligodendrocytes in the ICH brain are described. Finally, the clinical and translational implications of microglial polarization in ICH are presented, including the evidence that therapeutic approaches aimed at modulating microglial function might mitigate ICH injury and improve brain repair.

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“…Furthermore, there is evidence for the role of transforming growth factor-β (TGF-β), a profibrotic cytokine, in the regulation of hyaluronan production (Heldin et al, 1989;Westergren-Thorsson et al, 1990;Dubaybo and Thet, 1990). Tissue injury, including cerebral injury, leads to significant increase in TGF-β locally (Logan et al, 1992;Wang et al, 1995), where it may play a role in anti-inflammatory processes and in brain tissue remodeling, as well as in the serum (Kaestner and Dimitriou, 2013;Shi et al, 2015), where it may trigger catabolic signaling for muscle atrophy (Springer et al, 2014;Budasz-Rwiderska et al, 2005), stimulate the production of hyaluronan (Al'Qteishat et al, 2006), and the migration (Samuel et al, 1993) and differentiation of myofibroblasts leading to fibrosis (Webber et al, 2009a(Webber et al, , 2009b. Moreover, catabolism of hyaluronan by hyaluronidases (Colombaro et al, 2015), and TGF-β antagonism (Midgley et al, 2015) can reduce the levels of accumulated hyaluronan, potentially disrupting progression to fibrosis.…”

Section: Discussionmentioning

confidence: 99%

Human recombinant hyaluronidase injections for upper limb muscle stiffness in individuals with cerebral injury: A case series

Raghavan

Mirchandani

et al. 2018

Journal of Bodywork and Movement Therapies

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Increased frequency of circulating regulatory T cells in patients with acute cerebral hemorrhage

Cited by 21 publications

References 25 publications

Changes in the cellular immune system and circulating inflammatory markers of stroke patients

Changes in the cellular immune system and circulating inflammatory markers of stroke patients

Modulators of microglial activation and polarization after intracerebral haemorrhage

Human recombinant hyaluronidase injections for upper limb muscle stiffness in individuals with cerebral injury: A case series

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