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The PD-1/PD-Ls pathway is up-regulated during the suppression of experimental autoimmune encephalomyelitis treated by Astragalus polysaccharides.

08:00 EDT 1st April 2019 | BioPortfolio

Summary of "The PD-1/PD-Ls pathway is up-regulated during the suppression of experimental autoimmune encephalomyelitis treated by Astragalus polysaccharides."

Multiple sclerosis (MS) is an inflammatory demyelinating disease of CNS. Astragalus polysaccharides (APS), the main active extract from astragalus membranaceus which is a kind of traditional Chinese medicinal herb, is associated with a variety of immunomodulatory activities. We have evaluated the therapeutic effects of APS in the animal model of MS, experimental autoimmune encephalomyelitis (EAE). It was found that APS could effectively alleviate EAE through inhibiting MOG-specific T cell proliferation and reducing the expression of proinflammatory cytokines, which is mediated by up-regulating the expression of PD-1/PD-Ls signaling pathway. Our results demonstrated that EAE could be suppressed significantly by APS administration. It indicated that APS might be a potential of developing innovative drug for the therapy of MS.

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This article was published in the following journal.

Name: Journal of neuroimmunology
ISSN: 1872-8421
Pages: 78-90

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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).

An experimental animal model for central nervous system demyelinating disease. Inoculation with a white matter emulsion combined with FREUND'S ADJUVANT, myelin basic protein, or purified central myelin triggers a T cell-mediated immune response directed towards central myelin. The pathologic features are similar to MULTIPLE SCLEROSIS, including perivascular and periventricular foci of inflammation and demyelination. Subpial demyelination underlying meningeal infiltrations also occurs, which is also a feature of ENCEPHALOMYELITIS, ACUTE DISSEMINATED. Passive immunization with T-cells from an afflicted animal to a normal animal also induces this condition. (From Immunol Res 1998;17(1-2):217-27; Raine CS, Textbook of Neuropathology, 2nd ed, p604-5)

A group of 7 proteins produced from a single gene by alternate splicing found in central and peripheral nervous system myelin. The major basic protein (MBP) has long been of interest because it is the antigen, that, when injected into an animal, elicits a cellular immune response that produces the CNS autoimmune disease called experimental allergic encephalomyelitis (ENCEPHALOMYELITIS, ALLERGIC). In the peripheral nervous system, myelin basic protein 18.5-kDa is often referred to as the P1 protein. (From Siegel et al., Basic Neurochemistry, 5th ed, p130, 133)

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)

An experimental animal model for the demyelinating disease of GUILLAINE-BARRE SYNDROME. In the most frequently used protocol, animals are injected with a peripheral nerve tissue protein homogenate. After approximately 2 weeks the animals develop a neuropathy secondary to a T cell-mediated autoimmune response directed towards the MYELIN P2 PROTEIN in peripheral nerves. Pathologic findings include a perivascular accumulation of macrophages and T lymphocytes in the peripheral nervous system, similar to that seen in the Guillaine-Barre syndrome. (From Adams et al., Principles of Neurology, 6th ed, p1314; J Neuroimmunol 1998 Apr 1;84(1):40-52)

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