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Human Mannose-binding Lectin in Immunity: Friend, Foe, or Both?
Jean-Laurent Casanova1, Laurent Abel
1Pediatric Hematology-Immunology Unit, Necker Enfants-Malades Hospital, Paris, France. casanova@necker.fr
The Journal of Experimental Medicine
|May 19, 2004
Summary
Human mannose-binding lectin (MBL) is a key part of innate immunity, but studies show individuals lacking functional MBL are not prone to severe infections, suggesting it may be redundant.
Area of Science:
- Immunology
- Microbiology
- Genetics
Background:
- Human mannose-binding lectin (MBL) is a crucial pattern recognition molecule in the innate immune system.
- MBL initiates the lectin pathway of complement activation, a primitive defense mechanism against pathogens.
- A significant portion of the human population (approximately 5%) possesses genetic variations leading to a lack of functional serum MBL.
Purpose of the Study:
- To investigate the immunological significance of human mannose-binding lectin (MBL).
- To determine if the absence of functional MBL impacts susceptibility to infections.
- To evaluate the evolutionary role of MBL in human populations.
Main Methods:
- Review of prospective studies on individuals with and without functional MBL.
- Analysis of infection rates and severity in different MBL genotypes.
- Comparative analysis of immune responses in MBL-deficient versus MBL-sufficient individuals.
Main Results:
- Individuals lacking functional serum MBL do not exhibit increased susceptibility to severe infections.
- Prospective studies have not identified a significant clinical disadvantage for MBL-deficient individuals.
- These findings challenge the presumed essential role of MBL in protective immunity.
Conclusions:
- Human MBL appears to be largely redundant for effective protective immunity against common infections.
- The lack of a clear disadvantage in MBL-deficient individuals suggests MBL may not be under strong positive selection for pathogen defense.
- There is a possibility that MBL has been subject to counter-selection due to potential deleterious effects.