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Lack of association of mannose binding lectin variant alleles with systemic lupus erythematosus
  1. T Momot,
  2. K Ahmadi-Simab,
  3. A Gause,
  4. W L Gross,
  5. E Gromnica-Ihle,
  6. H H Peter,
  7. K Manger,
  8. H Zeidler,
  9. R E Schmidt,
  10. T Witte
  1. Abteilung Klinische Immunologie, Medizinische Hochschule Hannover, Carl-Neuberg-Str 1, 30625 Hannover, Germany
  1. Correspondence to:
    Dr T Witte
    witte.torsten{at}mh-hannover.de

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Mannose binding lectin (MBL) is a member of the collectin family, is structurally related to the complement component C1q, and is involved in the innate immune response.1 So far, three mutations of MBL have been described in codons 54, 57, and 52 (termed variant alleles B, C, and D or 0 alleles) that are associated with dysfunctional formation of the molecule.2,3 Homozygous combinations of variant alleles of MBL have been found in about 1–10% of Europeans and are associated with increased incidence of infections in childhood, subsets of adults, and possibly those with systemic lupus erythematosus (SLE).4

In a recent prospective study of 91 patients with SLE, MBL deficiency was a risk factor for “arterial thrombosis”, in particular, with myocardial infarction.5

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