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  • Deficiency for mannan-binding lectin is associated with antibodies to Saccharomyces cerevisiae in patients with Crohn’s disease and their relatives

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Deficiency for mannan-binding lectin is associated with antibodies to Saccharomyces cerevisiae in patients with Crohn’s disease and their relatives
  1. F Seibold1,
  2. A B W Boldt2,
  3. B Seibold-Schmid3,
  4. A M Schoepfer3,
  5. B Flogerzi3,
  6. S Müller3,
  7. J F J Kun4
  1. 1Division of Gastroenterology, Inselspital, University of Bern, Bern, Switzerland
  2. 2Institute for Tropical Medicine, Department of Parasitology, Tübingen, Germany
  3. 3Division of Gastroenterology, Inselspital, University of Bern, Bern, Switzerland
  4. 4Institute for Tropical Medicine, Department of Parasitology, Tübingen, Germany
  1. Correspondence to:
    F Seibold
    Division of Gastroenterology, University Hospital of Bern, Freiburgstrasse, CH 3010 Bern, Switzerland;frank.seibold{at}insel.ch

https://doi.org/10.1136/gut.2006.110007

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    Mannan-binding lectin (MBL) is a member of the collectin family and is an important component of the innate immune response. Three different MBL alleles in coding exon 1 (point mutations in codons 52, 54 and 57) result in low serum levels of MBL.1 Earlier, we described cellular and humoral immune reactivity of a subgroup of patients with Crohn’s disease to mannans, a cell wall antigen of yeasts.2 The humoral immune response in these patients is commonly known as antibodies to Saccharomyces cerevisiae (ASCA). In a previous paper, we found considerably more patients with Crohn’s disease with low MBL serum levels to be ASCA positive than in the subgroup with high MBL levels. The homozygotic or compound heterozygotic mutations in the exon were associated with the development of ASCA in patients with Crohn’s disease.3

    This is in contrast with the data reported in this journal by …

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    Footnotes

    • Funding: This work was supported by the Swiss National Science Foundation SNSF 3200B0-107527/1 and the Swiss National Science Foundation SNSF 3347 CO-108792.

    • Competing interests: None.

    • ABWB was supported by a PhD scholarship from the CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico, Brazil).