Association of CLEC16A with human common variable immunodeficiency disorder and role in murine B cells

@inproceedings{Li2015AssociationOC,
  title={Association of CLEC16A with human common variable immunodeficiency disorder and role in murine B cells},
  author={Jin Li and Silje F J{\o}rgensen and Solrun Melkorka Maggadottir and Marina Bakay and Klaus Warnatz and Joseph T. Glessner and Rahul Pandey and Ulrich Salzer and Reinhold Ernst Schmidt and Elena P{\'e}rez and Elena S. Resnick and Sigune Goldacker and Mary Buchta and Torsten Witte and Leonid Padyukov and V. Videm and Trine Folseraas and Faranaz Atschekzei and James T. Elder and Rajan P. Nair and Juliane Winkelmann and Christian Gieger and Markus M. N{\"o}then and Carsten Buening and Stephan Brand and Kathleen E Sullivan and Jordan S Orange and B{\o}rre Fevang and Stefan Schreiber and Wolfgang Lieb and P. A. Aukrust and HelenM. Chapel and Charlotte Cunningham-Rundles and Andre Franke and Tom H. Karlsen and Bodo Grimbacher and Hakon Hakonarson and Lennart Hammarstr{\"o}m and Eva Ellinghaus},
  booktitle={Nature communications},
  year={2015}
}
Common variable immunodeficiency disorder (CVID) is the most common symptomatic primary immunodeficiency in adults, characterized by B-cell abnormalities and inadequate antibody response. CVID patients have considerable autoimmune comorbidity and we therefore hypothesized that genetic susceptibility to CVID may overlap with autoimmune disorders. Here, in the largest genetic study performed in CVID to date, we compare 778 CVID cases with 10,999 controls across 123,127 single-nucleotide… CONTINUE READING
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