Tim-4 expression increases in ischemic stroke patients and is associated with poor outcome

Xu, Lixiang; Ye, Zhinan; Wang, Binda; Huang, Ying; Zhou, Lin; Liu, Chunyan; Chen, Dongdong; Sun, Menghong; Dai, Fangyu; Guan, Shuyi; Tang, Weiguo

doi:10.1016/j.jneuroim.2017.11.017

Cited by 8 publications

(7 citation statements)

References 26 publications

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“…Furthermore, stroke severity was positively correlated with sTim-4 levels in plasma. Up-regulated sTim-4 in plasma might act as a prognostic biomarker of ischemic stroke (98). In addition, serum levels of sTim-4 were significantly increased in ankylosing spondylitis patients, which was positively correlated with TNFα levels and Bath ankylosing spondylitis disease activity index (99).…”

Section: Soluble Tim-4mentioning

confidence: 93%

Tim-4 in Health and Disease: Friend or Foe?

Liang

et al. 2020

Front. Immunol.

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T-cell immunoglobulin and mucin domain containing 4 (Tim-4) is a phosphatidylserine receptor and is selectively expressed on antigen presenting cells. Recently, Tim-4 was reported to be expressed on iNKT cells, B1 cells, and tumor cells, suggesting it has multiple biological functions. In this review, we mainly summarize the expression and regulation of Tim-4 in immune cells including T cells, macrophages, dendritic cells, NKT cells, B cells, and mast cells. The expression of Tim-4 in these cells implies that Tim-4 might participate in immune related diseases. Emerging evidence emphasizes a substantial role for Tim-4 in maintaining homeostasis by regulating various immune responses, including viral infection, allergy, autoimmunity, and tumor immunity. Here, we collectively evaluated the role of Tim-4 in health and diseases. This summary will be extremely useful to fully understand the function of Tim-4 in the pathogenesis of immune related diseases, which would provide novel clues for the diagnosis and treatment of diseases.

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Section: Soluble Tim-4mentioning

confidence: 93%

Tim-4 in Health and Disease: Friend or Foe?

Liang

et al. 2020

Front. Immunol.

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“…Accumulating evidence has shown that the TIM‐4 pathway plays an important role in IRI . TIM‐4 expression is also increased in ischaemic stroke patients . Thus, we hypothesized that TIM‐4 might participate in cerebral IRI.…”

Section: Discussionmentioning

confidence: 97%

“…10,12,22 TIM-4 expression is also increased in ischaemic stroke patients. 26 Thus, we hypothesized that TIM-4 might participate in cerebral IRI. To test this hypothesis, we es- Accumulating evidence shows that ischaemic injury and inflammation account for the pathogenic progression of stroke.…”

Section: Discussionmentioning

confidence: 99%

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Inhibition of TIM‐4 protects against cerebral ischaemia‐reperfusion injury

Zheng

Huang

Wang

et al. 2019

J Cellular Molecular Medi

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TIM-4 plays an important role in ischaemia-reperfusion injury of liver and kidney; however, the effects of TIM-4 on cerebral ischaemia-reperfusion injury (IRI) are unknown. The purpose of the present study was to investigate the potential role of TIM-4 in experimental brain ischaemia-reperfusion injury. In this study, cerebral ischaemia reperfusion was induced by transient middle cerebral artery occlusion (MCAO) for 1 hour in C57/BL6 mice. The TIM-4 expression was detected in vivo or vitro by real-time quantitative polymerase chain reaction, Western blot and flow cytometric analysis. In vivo, the administration of anti-TIM-4 antibodies significantly suppressed apoptosis, inhibited inflammatory cells and enhanced anti-inflammatory responses. In vitro, activated microglia exhibited reduced cellular proliferation and induced IRI injury when co-cultured with neurons; these effects were inhibited by anti-TIM-4 antibody treatment. Similarly, microglia transfected with TIM-4 siRNA and stimulated by LPS + IFN-γ alleviated the TIM-4-mediated damage to neurons.Collectively, our data indicate that the inhibition of TIM-4 can improve the inflammatory response and exerts a protective effect in cerebral ischaemia-reperfusion injury. K E Y W O R D Scerebral ischaemia-reperfusion injury, co-culture, TIM-4

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“…Expression of the antigen presenting molecule HLA-DR on monocytes is diminished in stroke patients and correlates with incidence of stroke associated infection [15,177]. Likewise, increased monocytic expression of Tim-4, a molecule with T cell costimulatory capacity, correlated with poor outcome in ischaemic stroke patients [178]. Both HLA-DR and Tim-4 are critical mediators of T cell activation in response to antigen, suggesting the initiation of adaptive immunity may be impaired in stroke.…”

Section: Myeloid Cell Function and Trainingmentioning

confidence: 99%

Systemic innate myeloid responses to acute ischaemic and haemorrhagic stroke

et al. 2022

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Acute ischaemic and haemorrhagic stroke account for significant disability and morbidity burdens worldwide. The myeloid arm of the peripheral innate immune system is critical in the immunological response to acute ischaemic and haemorrhagic stroke. Neutrophils, monocytes, and dendritic cells (DC) contribute to the evolution of pathogenic local and systemic inflammation, whilst maintaining a critical role in ongoing immunity protecting against secondary infections. This review aims to summarise the key alterations to myeloid immunity in acute ischaemic stroke, intracerebral haemorrhage (ICH), and subarachnoid haemorrhage (SAH). By integrating clinical and preclinical research, we discover how myeloid immunity is affected across multiple organ systems including the brain, blood, bone marrow, spleen, and lung, and evaluate how these perturbations associate with real-world outcomes including infection. These findings are placed in the context of the rapidly developing field of human immunology, which offers a wealth of opportunity for further research.

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Tim-4 expression increases in ischemic stroke patients and is associated with poor outcome

Cited by 8 publications

References 26 publications

Tim-4 in Health and Disease: Friend or Foe?

Tim-4 in Health and Disease: Friend or Foe?

Inhibition of TIM‐4 protects against cerebral ischaemia‐reperfusion injury

Systemic innate myeloid responses to acute ischaemic and haemorrhagic stroke

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