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Promotion of microglial phagocytosis by tuftsin stimulates remyelination in experimental autoimmune encephalomyelitis.

08:00 EDT 31st October 2019 | BioPortfolio

Summary of "Promotion of microglial phagocytosis by tuftsin stimulates remyelination in experimental autoimmune encephalomyelitis."

Microglia were once thought to serve a pathogenic role in demyelinating diseases, particularly in multiple sclerosis (MS). However, it has recently been shown that in the experimental autoimmune encephalomyelitis (EAE) model of MS, microglia could serve a protective role by promoting remyelination via the efficient removal of apoptotic cells, the phagocytosis of debris and the support of myelinating oligodendrocytes. The aim of the present study was to determine if the effect of microglia could promote the recovery of EAE and attenuate symptoms in EAE. The severity of EAE was assessed by clinical scores, pathologic changes revealed by luxol fast blue staining and immunohistochemical techniques. The results suggested that microglia reduced clinical scores in mice, suppressed ongoing severe EAE and promoted remyelination and recovery in EAE mice. In addition, following induction with tuftsin, the M1/M2 cytokine balance was shifted, downregulating the proinflammatory M1 response and upregulating the anti‑inflammatory M2 response. Generally, microglia can stimulate remyelination, which serves a protective role in different phases of EAE and may represent a potential therapeutic strategy for the treatment of MS.

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Name: Molecular medicine reports
ISSN: 1791-3004
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Medical and Biotech [MESH] Definitions

Experimental animal models for human AUTOIMMUNE DISEASES OF THE NERVOUS SYSTEM. They include GUILLAIN-BARRE SYNDROME (see NEURITIS, AUTOIMMUNE, EXPERIMENTAL); MYASTHENIA GRAVIS (see MYASTHENIA GRAVIS, AUTOIMMUNE, EXPERIMENTAL); and MULTIPLE SCLEROSIS (see ENCEPHALOMYELITIS, AUTOIMMUNE, EXPERIMENTAL).

Any autoimmune animal disease model used in the study of MYASTHENIA GRAVIS. Injection with purified neuromuscular junction acetylcholine receptor (AChR) (see RECEPTORS, CHOLINERGIC) components results in a myasthenic syndrome that has acute and chronic phases. The motor endplate pathology, loss of acetylcholine receptors, presence of circulating anti-AChR antibodies, and electrophysiologic changes make this condition virtually identical to human myasthenia gravis. Passive transfer of AChR antibodies or lymphocytes from afflicted animals to normals induces passive transfer experimental autoimmune myasthenia gravis. (From Joynt, Clinical Neurology, 1997, Ch 54, p3)

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The reforming of the MYELIN SHEATH around AXONS following loss due to injury or DEMYELINATING DISEASES.

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