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Reexamining the role of TACI coding variants in common variable immunodeficiency and selective IgA deficiency

Nature Genetics volume 39, pages 429–430 (2007)Cite this article

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Tumor necrosis factor (TNF)-like receptors are members of a superfamily of proteins involved in regulating maturation and survival of lymphocytes. One of these receptors, TACI (transmembrane activator and CAML interactor; encoded by TNFRSF13B), binds two ligands, BAFF and APRIL. Deletion of Tnfrsf13b in mice results in an impaired response to thymus-independent antigens1 and virtually abolishes APRIL-induced switching to IgA, IgE and IgG1 (ref. 2). Conversely, lack of APRIL, owing to a targeted inactivation of Tnfsf13 in mice, results in an impaired ability to switch to IgA production3.

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Acknowledgements

We are indebted to C. Lindgren (core facility at the Kliniskt forskningscentrum, Karolinska Institute); J. Birmelin (University of Freiburg); S. Buckridge and A. Thrasher (Institute of Child Health) for the mutation analyses; R. Engqvist (Division of Clinical Immunology, Karolinska University Hospital Huddinge) for collection of family samples and A. Schaffer (National Center for Biotechnology Information, US National Institutes of Health) for statistical advice. This work was supported by ALF funding from the Stockholm County Council, the Swedish Research Council, the Deutsche Forschungsgemeinschaft (DFG) grant SFB620/C2, USIDnet grant NO1-A1-30070, the Primary Immunodeficiency Association, the Medical Research Council UK and European Union grant SP23-CT-2005-006411.

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Author notes

  1. Qiang Pan-Hammarström and Ulrich Salzer: These authors contributed equally to this work.

Authors and Affiliations

  1. Division of Clinical Immunology, Karolinska University Hospital Huddinge, Stockholm, SE-14186, Sweden

    Qiang Pan-Hammarström, Likun Du & Lennart Hammarström

  2. Division of Rheumatology and Clinical Immunology, Medical Center, University Hospital, Hugstetterstrasse 55, Freiburg, D-79106, Germany

    Ulrich Salzer

  3. Department of Respiratory Medicine and Allergy, Immunodeficiency Unit, Sahlgrenska University Hospital, Gothenburg, SE-41345, Sweden

    Janne Björkander

  4. Division of Clinical Immunology, Mount Sinai Medical Center, New York, 10029, New York, USA

    Charlotte Cunningham-Rundles

  5. Center for Cancer Research, National Cancer Institute, US National Institutes of Health, Bethesda, 20892, Maryland, USA

    David L Nelson

  6. Molecular Immunology Unit, Institute of Child Health, London, WC1N 1EH, UK

    Chiara Bacchelli & H Bobby Gaspar

  7. Center for Immunology, University of Minnesota Medical School, Minneapolis, 55455, Minnesota, USA

    Steven Offer & Timothy W Behrens

  8. Department of Immunology, Royal Free Hospital, University College London, London, 3NW 2QG, UK

    Bodo Grimbacher

Authors
  1. Qiang Pan-Hammarström
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  2. Ulrich Salzer
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  11. Bodo Grimbacher
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  12. Lennart Hammarström
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Corresponding authors

Correspondence to Qiang Pan-Hammarström or Lennart Hammarström.

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Supplementary information

Supplementary Fig. 1

Mutations in TNFRSF13B in families with IgAD. (PDF 90 kb)

Supplementary Table 1

Mutations and sequence variants in TNFRSF13B in individuals with CVID and IgAD. (PDF 82 kb)

Supplementary Table 2

Primer sequences for detection of TNFRSF13B mutation and sequence variants using a SNP-based mutation assay. (PDF 67 kb)

Supplementary Table 3

Lack of correlation between heterozygous TNFRSF13B mutations and sequence variants and IgA deficiency. (PDF 67 kb)

Supplementary Note (PDF 66 kb)

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Pan-Hammarström, Q., Salzer, U., Du, L. et al. Reexamining the role of TACI coding variants in common variable immunodeficiency and selective IgA deficiency. Nat Genet 39, 429–430 (2007). https://doi.org/10.1038/ng0407-429

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