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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis

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Mannose binding lectin mediated complement pathway in multiple sclerosis.

Janet Y Kwok¹, Florin Vaida, Ryan M Augst

¹Department of Pediatrics, University of California-San Diego, La Jolla, CA 92093, United States.

Journal of Neuroimmunology

|September 14, 2011

Summary

The mannose binding lectin (MBL) complement pathway may be activated in multiple sclerosis (MS). Higher levels of MBL and MASP-2 were found in MS patients, suggesting a role in disease progression.

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Area of Science:

Immunology
Neuroimmunology
Complement System

Background:

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system.
The innate immune system, including the complement cascade, plays a role in MS pathogenesis.
Mannose binding lectin (MBL) is a key initiator of the lectin complement pathway.

Purpose of the Study:

To investigate the role of the mannose binding lectin (MBL) complement activation pathway in multiple sclerosis (MS).
To analyze the expression of MBL, MBL-associated serine protease-2 (MASP-2), and functional MBL/MASP-2 mediated C4 cleavage (fMBL) in MS patients and controls.

Main Methods:

Analysis of plasma and cerebrospinal fluid (CSF) samples from 87 MS patients and non-MS controls.
Quantification of MBL, MASP-2, and fMBL levels using established assays.
Statistical comparison of MBL pathway components between MS and control groups, including MS subtypes.

Main Results:

Significantly higher median plasma levels of fMBL and MASP-2 were observed in MS patients compared to non-MS controls.
These elevated levels of fMBL and MASP-2 in MS were consistent across different subtypes of the disease.
The findings indicate a potential association between MBL complement pathway activation and MS.

Conclusions:

The mannose binding lectin (MBL) complement pathway appears to be activated in multiple sclerosis (MS).
Elevated MBL and MASP-2 levels suggest a potential contribution to MS risk or disease progression.
Further research is warranted to elucidate the precise role of the MBL pathway in MS pathogenesis.