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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
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Tissue microarray methodology identifies complement pathway activation and dysregulation in progressive multiple

Sam Loveless1, James W Neal2, Owain W Howell3

  • 1Division of Psychological Medicine and Clinical Neurology, Cardiff University, Cardiff, CF14 4XN, United Kingdom.

Brain Pathology (Zurich, Switzerland)
|July 15, 2017
PubMed
Summary
This summary is machine-generated.

Complement pathway proteins are dysregulated in both white and grey matter lesions in Multiple Sclerosis (MS). This study quantifies complement involvement, revealing potential biomarkers for disease progression.

Keywords:
complementimmunohistochemistrymultiple sclerosistissue microarray

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Area of Science:

  • Neuroimmunology
  • Complement System Biology

Background:

  • The complement pathway's role in Multiple Sclerosis (MS) white matter (WM) and grey matter (GM) pathology is implicated but not quantitatively assessed.
  • Understanding complement involvement is crucial for developing targeted MS therapies.

Purpose of the Study:

  • To quantitatively assess the localization and expression of complement pathway proteins and regulators in progressive MS cortical GM and subcortical WM.
  • To investigate the correlation between complement activation and regulatory protein expression in MS lesions.

Main Methods:

  • Tissue MicroArray (TMA) methodology combined with immunohistochemistry.
  • Quantitative analysis of complement proteins (C1q, C3b, C5aR) and regulators (C1INH, CR1, FH, clusterin) in WM and GM lesions versus normal-appearing tissue.
  • Utilized standard pathology markers and digitized slides for analysis.

Main Results:

  • Increased C1q, C3b, C5aR, HLA-DR, and GFAP in WM lesions (WML) and GM lesions (GML) compared to normal-appearing WM (NAWM) and GM (NAGM).
  • Complement regulators were more abundant in WM lesions; however, GM lesions showed increased C1q+ neurons and decreased complement regulator-expressing neurons.
  • Correlation between complement components and regulators in WM, but not in GM, indicating distinct regulatory mechanisms.

Conclusions:

  • TMA and quantitative analysis demonstrate complement dysregulation in MS GM lesions, with C1q+ cell density associated with tissue lesions.
  • Complement activation and dysregulation are confirmed in all progressive MS cases.
  • The complement system presents potential biomarkers for MS disease progression.