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Related Concept Videos

Complement System01:27

Complement System

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The complement system is a group of approximately 20 plasma proteins that strengthen the body's defenses against infections through opsonization, inflammation, and cell lysis. Opsonization involves coating pathogens with complement proteins, making them more recognizable and facilitating phagocyte engulfment. Certain complement proteins induce inflammation that attracts immune cells to the site of infection. Cell lysis involves the destruction of pathogens through the formation of a...
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Related Experiment Video

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Induction of Paralysis and Visual System Injury in Mice by T Cells Specific for Neuromyelitis Optica Autoantigen Aquaporin-4
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Mannose-binding Lectin Mediated Complement Pathway in Autoimmune Neurological Disorders.

Mehrdad Farrokhi1, Mehrnoosh Dabirzadeh2, Nastaran Dastravan3

  • 1Department of Immunology, School of Medicine, Isfahan University of Medical Sciences, Isfahan, Iran.

Iranian Journal of Allergy, Asthma, and Immunology
|July 18, 2016
PubMed
Summary
This summary is machine-generated.

Mannose-binding lectin (MBL) levels correlate with disease severity in multiple sclerosis (MS), Guillain-Barre Syndrome (GBS), and myasthenia gravis (MG). This suggests MBL

Keywords:
AutoimmunityComplement system proteinsGuillain-Barre syndromeMannose-binding lectinMultiple sclerosisMyasthenia gravis

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Area of Science:

  • Immunology
  • Neurology
  • Autoimmune Diseases

Background:

  • Multiple sclerosis (MS), Guillain-Barre Syndrome (GBS), and Myasthenia gravis (MG) are distinct autoimmune neurological disorders.
  • Complement system activation is implicated in the pathogenesis of MS, GBS, and MG.
  • The role of mannose-binding lectin (MBL) as an immunopathogenesis biomarker and its association with disease severity in these conditions remain under-investigated.

Purpose of the Study:

  • To investigate plasma levels of mannose-binding lectin (MBL) in patients with MS, GBS, and MG.
  • To assess the association between MBL levels and the clinical severity of these neurological diseases.

Main Methods:

  • A case-control study was conducted with 120 MS patients, 30 GBS patients, 30 MG patients, and 100 healthy controls.
  • Plasma MBL levels were quantified using enzyme-linked immunosorbent assay (ELISA).
  • Disease severity was assessed using established clinical scales: Expanded Disability Status Scale (EDSS) for MS, Quantitative Myasthenia Gravis Score (QMGS) for MG, and GBS Disability Scale (GDS) for GBS.

Main Results:

  • Significantly different mean plasma MBL levels were observed between patient groups and healthy controls (p<0.001).
  • Positive correlations were found between MBL plasma levels and disease severity scores: EDSS (r=+0.60, p<0.001), QMGS (r=+0.56, p=0.01), and GDS (r=+0.37, p=0.04).

Conclusions:

  • Mannose-binding lectin (MBL) may contribute to the pathogenesis and severity of MS, GBS, and MG through complement activation.
  • MBL shows potential as a biomarker for disease severity in these neurological autoimmune conditions.
  • Further research is needed to fully elucidate the underlying mechanisms of MBL's involvement in the lectin pathway's role in these diseases.