A hypermorphic IκBα mutation is associated with autosomal dominant anhidrotic ectodermal dysplasia and T cell immunodeficiency

نویسندگان

  • Gilles Courtois
  • Asma Smahi
  • Janine Reichenbach
  • Rainer Döffinger
  • Caterina Cancrini
  • Marion Bonnet
  • Anne Puel
  • Christine Chable-Bessia
  • Shoji Yamaoka
  • Jacqueline Feinberg
  • Sophie Dupuis-Girod
  • Christine Bodemer
  • Susanna Livadiotti
  • Francesco Novelli
  • Paolo Rossi
  • Alain Fischer
  • Alain Israël
  • Arnold Munnich
  • Françoise Le Deist
  • Jean-Laurent Casanova
چکیده

The Journal of Clinical Investigation | October 2003 | Volume 112 | Number 7 Introduction Patients with anhidrotic ectodermal dysplasia with immunodeficiency (EDA-ID) present with impaired development of skin appendices, resulting in sparse hair, conical teeth, and anhidrosis/hypohidrosis. Host defense is also impaired, resulting principally in multiple and severe bacterial diseases (1). X-linked EDA-ID (XL-EDA-ID) is caused by hypomorphic mutations in the gene encoding NEMO/IKKγ, the regulatory subunit of the IκB kinase (IKK) complex (1–8). IKK norA hypermorphic IκBα mutation is associated with autosomal dominant anhidrotic ectodermal dysplasia and T cell immunodeficiency

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Diagnosis and treatment in anhidrotic ectodermal dysplasia with immunodeficiency.

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Autosomal Recessive Hypohidrotic Ectodermal Dysplasia Caused by a Novel Mutation in EDAR Gene

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Somatic mosaicism has been described in several primary immunodeficiency diseases and causes modified phenotypes in affected patients. X-linked anhidrotic ectodermal dysplasia with immunodeficiency (XL-EDA-ID) is caused by hypomorphic mutations in the NF-κB essential modulator (NEMO) gene and manifests clinically in various ways. We have previously reported a case of XL-EDA-ID with somatic mosa...

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تاریخ انتشار 2003