Inherited Interleukin 2–Inducible T-Cell (ITK) Kinase Deficiency in Siblings With Epidermodysplasia Verruciformis and Hodgkin Lymphoma. (19th February 2019)

• Record Type: Journal Article
• Authors: Youssefian, Leila; Vahidnezhad, Hassan; Yousefi, Mehdi; Saeidian, Amir Hossein; Azizpour, Arghavan; Touati, Andrew; Nikbakht, Neda; Hesari, Kambiz Kamyab-; Adib-Sereshki, Mohammad Mahdi; Zeinali, Sirous; Mansoori, Behzad; Jazayeri, Ali; Karamzadeh, Razieh; Fortina, Paolo; Jouanguy, Emmanuelle; Casanova, Jean-Laurent; Uitto, Jouni
• Is Part Of: Clinical infectious diseases. Volume 68:Number 11(2019)
• Page Start: 1938
• Page End: 1941
• Publication Date: 2019-02-19
• Subjects: epidermodysplasia verruciformis -- immunodeficiency -- ITK -- human papillomavirus -- EBV infection; Communicable diseases -- Periodicals; 616.905
• DOI: 10.1093/cid/ciy942
• Languages: English
• ISSNs: 1058-4838

Abstract

Abstract: Biallelic mutations in the ITK gene cause a T-cell primary immunodeficiency with Epstein-Barr virus (EBV)–lymphoproliferative disorders. We describe a novel association of a homozygous ITK mutation with β–human papillomavirus (HPV)–positive epidermodysplasia verruciformis. Thus, loss of function in ITK can result in broad dysregulation of T-cell responses to oncogenic viruses, including β-HPV and EBV.