@article{SauerbreiLangenhanBrandstaedtetal.2014,
  author    = {Sauerbrei, A. and Langenhan, T. and Brandst{\"a}dt, A. and Schmidt-Ott, R. and Krumbholz, A. and Girschick, H. and Huppertz, H. and Kaiser, P. and Liese, J. and Streng, A. and Niehues, T. and Peters, J. and Sauerbrey, A. and Schroten, H. and Tenenbaum, T. and Wirth, S. and Wutzler, P.},
  title     = {Prevalence of antibodies against influenza A and B viruses in children in Germany, 2008 to 2010},
  series = {Eurosurveillance},
  volume    = {19},
  journal   = {Eurosurveillance},
  number    = {5},
  issn      = {1560-7917},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-117347},
  pages     = {20687},
  year      = {2014},
  abstract  = {The prevalence of influenza A and B virus-specific IgG was determined in sera taken between 2008 and 2010 from 1,665 children aged 0-17 years and 400 blood donors in Germany. ELISA on the basis of whole virus antigens was applied. Nearly all children aged nine years and older had antibodies against influenza A. In contrast, 40\% of children aged 0-4 years did not have any influenza A virus-specific IgG antibodies. Eighty-six percent of 0-6 year-olds, 47\% of 7-12 year-olds and 20\% of 13-17 year-olds were serologically naive to influenza B viruses. By the age of 18 years, influenza B seroprevalence reached approximately 90\%. There were obvious regional differences in the seroprevalence of influenza B in Germany. In conclusion, seroprevalences of influenza A and influenza B increase gradually during childhood. The majority of children older than eight years have basal immunity to influenza A, while comparable immunity against influenza B is only acquired at the age of 18 years. Children aged 0-6 years, showing an overall seroprevalence of 67\% for influenza A and of 14\% for influenza B, are especially at risk for primary infections during influenza B seasons.},
  language  = {en}
}
@article{DirksHaaseCantaertetal.2022,
  author    = {Dirks, Johannes and Haase, Gabriele and Cantaert, Tineke and Frey, Lea and Klaas, Moritz and Rickert, Christian H. and Girschick, Hermann and Meffre, Eric and Morbach, Henner},
  title     = {A novel AICDA splice-site mutation in two siblings with HIGM2 permits somatic hypermutation but abrogates mutational targeting},
  series = {Journal of Clinical Immunology},
  volume    = {42},
  journal   = {Journal of Clinical Immunology},
  number    = {4},
  doi       = {10.1007/s10875-022-01233-5},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-324253},
  pages     = {771-782},
  year      = {2022},
  abstract  = {Hyper-IgM syndrome type 2 (HIGM2) is a B cell intrinsic primary immunodeficiency caused by mutations in AICDA encoding activation-induced cytidine deaminase (AID) which impair immunoglobulin class switch recombination (CSR) and somatic hypermutation (SHM). Whereas autosomal-recessive AID-deficiency (AR-AID) affects both CSR and SHM, the autosomal-dominant form (AD-AID) due to C-terminal heterozygous variants completely abolishes CSR but only partially affects SHM. AR-AID patients display enhanced germinal center (GC) reactions and autoimmune manifestations, which are not present in AD-AID, suggesting that SHM but not CSR regulates GC reactions and peripheral B cell tolerance. Herein, we describe two siblings with HIGM2 due to a novel homozygous AICDA mutation (c.428-1G > T) which disrupts the splice acceptor site of exon 4 and results in the sole expression of a truncated AID variant that lacks 10 highly conserved amino acids encoded by exon 4 (AID-ΔE4a). AID-ΔE4a patients suffered from defective CSR and enhanced GC reactions and were therefore indistinguishable from other AR-AID patients. However, the AID-ΔE4a variant only partially affected SHM as observed in AD-AID patients. In addition, AID-ΔE4a but not AD-AID patients revealed impaired targeting of mutational hotspot motives and distorted mutational patterns. Hence, qualitative defects in AID function and altered SHM rather than global decreased SHM activity may account for the disease phenotype in these patients.},
  language  = {en}
}