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Related Concept Videos

Myasthenia Gravis ll: Pathophysiology01:22

Myasthenia Gravis ll: Pathophysiology

The disease process of myasthenia gravis begins at the neuromuscular junction, where antibodies attack key proteins needed for muscle activation. This immune reaction weakens signal transmission, leading to the characteristic muscle fatigue and weakness that define the condition.Immune-Mediated DamageIn most individuals, antibodies target acetylcholine receptors (AChRs) on the postsynaptic membrane of muscle cells. By blocking acetylcholine binding, these antibodies prevent the nerve signal...
Multiple Sclerosis l: Introduction01:19

Multiple Sclerosis l: Introduction

Multiple sclerosis is a chronic autoimmune disease of the central nervous system (CNS) that affects the brain, spinal cord, and optic nerves. It is an inflammatory demyelinating disorder and a leading cause of neurological disability in young adults.EpidemiologyMS commonly begins between 20 and 40 years of age and is twice as common in women. Its exact cause remains unclear, but genetic susceptibility contributes, with higher risk in first-degree relatives and identical twins. A greater...
Myasthenia Gravis: Overview and Treatment01:20

Myasthenia Gravis: Overview and Treatment

Myasthenia gravis is a neuromuscular transmission disorder characterized by weakness and increased fatigability of skeletal muscles. It is an autoimmune disease affecting approximately one in 2000 people, where antibodies against the α1 subunit of nicotinic acetylcholine receptors are produced.
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Related Experiment Video

Updated: Jun 27, 2026

Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis
05:55

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Published on: December 1, 2023

Elevated ATG5 expression in autoimmune demyelination and multiple sclerosis.

Mehrdad Alirezaei1, Howard S Fox, Claudia T Flynn

  • 1Molecular and Integrative Neurosciences Department, The Scripps Research Institute, La Jolla, California 92037, USA. malireza@scripps.edu

Autophagy
|December 11, 2008
PubMed
Summary
This summary is machine-generated.

Autophagy-related gene 5 (Atg5) is upregulated in T cells during multiple sclerosis (MS) relapses. Increased Atg5 expression in T cells correlates with disease severity and may drive inflammatory demyelination in MS.

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Last Updated: Jun 27, 2026

Quantification of Autoreactive Antibodies in Mice upon Experimental Autoimmune Encephalomyelitis
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Flow Cytometric Analysis of Lymphocyte Infiltration in Central Nervous System during Experimental Autoimmune Encephalomyelitis
09:01

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Published on: November 17, 2020

Area of Science:

  • Neuroimmunology
  • Cellular and Molecular Neuroscience
  • Autophagy Research

Background:

  • Multiple sclerosis (MS) is a T cell-mediated inflammatory CNS disorder.
  • Prolonged T cell survival and proliferation are implicated in MS progression.
  • Autophagy-related gene 5 (Atg5) influences T cell survival.

Purpose of the Study:

  • To investigate the role of Atg5 expression in T cells within MS.
  • To correlate Atg5 levels with disease activity and severity in experimental autoimmune encephalomyelitis (EAE) and human MS.

Main Methods:

  • Quantitative real-time PCR and protein analysis in EAE mouse models.
  • Analysis of T cells from relapsing-remitting MS patients.
  • Immunofluorescent histochemistry on MS brain tissue.

Main Results:

  • Atg5 expression correlated with clinical disability in EAE mice.
  • Upregulation and post-translational modification of Atg5 were observed in EAE, correlating with severity.
  • Elevated Atg5 expression in T cells from active relapsing-remitting MS patients.
  • Encephalitogenic T cells in MS brain samples showed Atg5 expression.

Conclusions:

  • Increased T cell expression of Atg5 is associated with active MS.
  • Atg5 may contribute to inflammatory demyelination in multiple sclerosis.