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Mannose binding lectin: genetics and autoimmune disease.

Akito Tsutsumi¹, Reiko Takahashi, Takayuki Sumida

¹Division of Clinical Immunology, Graduate School of Comprehensive Human Sciences, University of Tsukuba 1-1-1, Tennodai, Tsukuba 305-8575, Ibaraki, Japan. atsutsum@md.tsukuba.ac.jp

Autoimmunity Reviews

|August 6, 2005

Summary

Mannose-binding lectin (MBL) deficiency increases infection risk in immunocompromised individuals and may be linked to autoimmune diseases like lupus. MBL gene typing could help assess patient risks.

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Area of Science:

Immunology
Genetics

Background:

Mannose-binding lectin (MBL) is a crucial innate immunity serum protein.
MBL deficiency is associated with increased risk for autoimmune diseases, particularly systemic lupus erythematosus (SLE).
MBL deficiency also heightens infection susceptibility in immunocompromised states.

Purpose of the Study:

To explore the clinical significance of MBL deficiency in autoimmune diseases.
To evaluate the utility of MBL gene typing and serum MBL measurement for risk assessment.

Main Methods:

Analysis of MBL gene polymorphisms and serum MBL concentrations.
Review of clinical data concerning MBL deficiency, infections, and autoimmune diseases.

Main Results:

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MBL concentration is significantly influenced by common MBL gene single nucleotide polymorphisms.

MBL deficiency may be a risk factor for atherosclerosis and arterial thrombosis in autoimmune patients.

The role of MBL in tissue injury and the significance of anti-MBL autoantibodies in SLE require further investigation.

Conclusions:

MBL gene typing or serum MBL measurement may aid in assessing infection risk for patients with autoimmune diseases undergoing immunosuppressive therapy.
The precise pathological and clinical roles of MBL in autoimmune diseases remain to be fully clarified.