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Previous Volume 349:554-560 August 7, 2003 Number 6 Next

	Since this article has no abstract, we have provided an extract of the first 100 words of the full text and any section headings.

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The complement system is part of the innate immune system and contributes to the establishment of adaptive immune responses.¹ The mannan-binding lectin pathway of the complement system is activated when mannan-binding lectin binds to carbohydrate structures on microorganisms.² This happens through autoactivation of the mannan-binding lectin–associated serine protease 2 (MASP-2), which then cleaves complement factors C4 and C2, generating the C3 convertase C4bC2b.^3,4 Activation of C3 initiates the alternative pathway and the formation of the membrane-attack complex. Complement fragments deposited on microorganisms facilitate phagocytosis and initiate inflammatory reactions. Like mannan-binding lectin, the recognition molecules L-ficolin and H-ficolin activate complement by . . . [Full Text of this Article]

Case Report

Methods

Reagents and Samples

Recombinant Proteins

Complement Analysis

Gene Sequencing

Results

Discussion

Source Information

From the Departments of Rheumatology (K.S.-P.) and Clinical Immunology (L.T.J., L.F.), Aarhus University Hospital; and the Department of Medical Microbiology and Immunology, University of Aarhus (S.T., M.G., M.M.-K., R.S., J.C.J.) — both in Aarhus, Denmark; Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, Oxford, United Kingdom (L.F.); and the Institute of Laboratory Medicine, Section of Microbiology, Immunology, and Glycobiology, University of Lund, Lund, Sweden (A.G.S.).

Drs. Fugger and Jensenius contributed equally to this article.

Address reprint requests to Dr. Thiel at the Department of Medical Microbiology and Immunology, University of Aarhus, 8000 Aarhus, Denmark, or at st@microbiology.au.dk.

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