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Research on IL-33 in central nervous system diseases

2020-12-07
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Some neurological diseases are seriously plaguing people’s lives and affecting people’s health. The lack of suitable animal models that can truly reproduce the pathology and characteristics of human diseases also severely restricts the understanding of disease mechanisms. Central nervous system disease models are of great significance for studying the pathogenesis of central nervous system diseases and exploring effective treatment methods. In recent years, more and more studies on animal models have found that IL-33 has a unique function and role in the central nervous system.

IL-33 is a bifunctional protein. It is both a pro-inflammatory cytokine and a nuclear factor with regulatory transcription function. It is used in various diseases such as allergies, autoimmune diseases, allergic diseases, cardiovascular diseases, infections and tumors. Take effect.

As the main part of the human nervous system, the central nervous system (CNS) includes the brain and spinal cord, responsible for receiving, integrating, processing and transmitting information throughout the body. The occurrence and development process of CNS disease and nerve cell apoptosis and necrosis, oxidative damage, inflammation, ischemia, demyelination, excitotoxic effects of astrocytes and oligodendrocytes, axon and gene changes, etc. A variety of pathophysiological mechanisms are related. Central nervous system disease models play an important role in studying the pathogenesis of central nervous system diseases and drug screening. The Pharmacodynamics Department of Medicilon has a professional central nervous system disease evaluation model, combined with PET-CT imaging technology, which can evaluate the effectiveness and safety of central nervous system drugs and its blood-brain barrier Penetration ability is tested.

IL-33 has a high content in spinal cord and brain tissues, and is mainly secreted by neurons, oligodendrocytes, astrocytes, and microglia. More and more studies have shown that IL-33 plays a certain role in the pathophysiological mechanisms of the central nervous system, autoimmune system, allergies and cardiovascular diseases through the ST2 signaling system. Tumor Suppressor 2 (ST2) was first discovered in 1989 by growth-stimulated fibroblasts and is a ligand for IL-33.

Studies have found that IL-33 axis may have regulatory and protective effects in the occurrence and development of central nervous system diseases, and IL-33 can be used as a new target for the treatment of central nervous system diseases. For example, Alzheimer’s disease is a devastating disease, a progressive and debilitating brain disease, which appears in the brain in the form of beta amyloid plaques (Aβ) and neurofibrillary tangles. During the course of the disease, the accumulation of ‘plaque’ and ‘tangles’ leads to the loss of connections between nerve cells, eventually nerve cells die and brain tissue is lost.

Microglial cells are a component of the body’s immune system and are responsible for purifying the central nervous system (CNS) and cleaning up plaques, damaged cells and other substances that need to be cleaned up. But microglia can also secrete certain compounds that induce neurotoxicity, which can poison astrocytes in the brain. This damage can lead to many neurological diseases, including multiple sclerosis.

Studies have found that IL-33 seems to work by mobilizing microglia to surround amyloid plaques, absorbing and digesting them, and reducing the number and size of plaques. IL-33 does this by inducing neprilysin, an enzyme known to degrade soluble amyloid. In addition, IL-33 treatment can work by inhibiting inflammation in brain tissue. Earlier studies have confirmed that inflammation promotes the formation of plaques and tangles. Therefore, IL-33 not only helps to remove the amyloid plaques that have formed, but also prevents the deposition of plaques and tangles in the first place.

The researcher said that it is currently unclear whether this study is related to human Alzheimer’s disease. But there are some encouraging clues. For example, some previous genetic studies have confirmed the association between IL-33 mutations and Alzheimer’s disease in European and Chinese populations. In addition, the brains of Alzheimer’s disease patients contain less IL-33 than non-Alzheimer’s disease patients.

With the gradual and in-depth study of IL-33, its mechanism of action in diseases will become clearer, which will help to further understand the relationship between IL-33 and central nervous system diseases, and provide a way to explore the treatment of central nervous system diseases.

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