Abstract

Ischemic stroke after cerebral artery occlusion is one of the major causes of chronic disability worldwide. Interleukins (ILs) play a bidirectional role in ischemic stroke through information transmission, activation and regulation of immune cells, mediating the activation, multiplication and differentiation of T and B cells and in the inflammatory reaction. Crosstalk between different ILs in different immune cells also impact the outcome of ischemic stroke. This overview is aimed to roughly discuss the multiple roles of ILs after ischemic stroke. The roles of IL-1, IL-2, IL-4, IL-5, IL-6, IL-8, IL-9, IL-10, IL-12, IL-13, IL-15, IL-16, IL-17, IL-18, IL-19, IL-21, IL-22, IL-23, IL-32, IL-33, IL-34, IL-37, and IL-38 in ischemic stroke were discussed in this review.

Highlights

  • Ischemic stroke after cerebral artery occlusion is one of the major causes of chronic disability worldwide, and there is still a lack of effective methods to improve functional recovery after cerebral stroke [1]

  • These findings indicate that IL-6 may be a predictor of the prognosis of ischemic stroke patients

  • A meta-analysis exploring the relationship between IL-10 gene polymorphism and ischemic stroke risk revealed no overall significant association of IL-10 with ischemic stroke risk, but an association was found with macrovascular disease and microvascular disease [71], demonstrating that certain subtypes of ischemic stroke are correlated to IL-10 gene polymorphisms

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Summary

INTRODUCTION

Ischemic stroke after cerebral artery occlusion is one of the major causes of chronic disability worldwide, and there is still a lack of effective methods to improve functional recovery after cerebral stroke [1]. Inflammatory interactions at the blood-endothelial interface, including adhesion molecules, cytokines, chemokines and white blood cells, are crucial for the pathogenesis of tissue injury in cerebral infarction [2]. IL, refers to a lymphocyte medium that interacts between white blood cells or immune cells. It is a cytokine in the same category as blood cell growth factor. Both IL and hemocyte growth factor belong to cytokines, and they coordinate and interact with each other to complete hematopoiesis and immune regulation functions together. This review is to discuss the inflammatory effects of IL in the pathogenesis of stroke, the interactions between different IL-mediated pathways, Interleukin Family in Ischemic Stroke the cell-type dependent effects of different mediators and how different ILs regulate complex inflammatory cascades. The role of IL-1, IL-4, IL-6, and IL-10 were discussed in more detail

IL-1 FAMILY
Mechanism of Pleiotropic Effects of IL-1 on Ischemic Stroke
The Mechanisms of IL-1b-Induced Brain Damage in Ischemic Stroke
IL-1b Aggravates the BBB Dysfunction
IL-1b Mediates the Inflammatory Response in Ischemic
IL-1b Promotes Apoptosis After Ischemic Stroke
IL-2 Expression Decreased After Ischemic Stroke
The Role of IL-2 in Ischemic Stroke
IL-4 Promotes the M2 Polarization of Microglia/Macrophages
Inhibition Pro-Inflammatory Cytokines
IL-4 Is Essential for Sex Differences in Vulnerability to
IL-4 Affects Neuronal Excitability
Dual Role of IL-6 in Ischemic Stroke
IL-8 IN ISCHEMIC STROKE
IL-10 in Ischemic Stroke
The Mechanism of IL-10 in Inhibiting Inflammatory Responses After Stroke
The Role of IL-10 in Neurogenesis After Ischemic Stroke Injection of activated
IL-12 AND ISCHEMIC STROKE
IL-13 AND ISCHEMIC STROKE
10 IL-15 AND ISCHEMIC STROKE
11 IL-16 IN ISCHEMIC STROKE
13 IL-19 AND ISCHEMIC STROKE
12 IL-18 IN ISCHEMIC STROKE
14 IL-20 IN ISCHEMIC STROKE
14.1 IL-20 Promotes Inflammation After Ischemic Stroke
16 IL-33 AND ISCHEMIC STROKE
17 OTHER ILS IN ISCHEMIC STROKE
Findings
18 CONCLUSIONS AND PERSPECTIVES
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