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Interaction between filaggrin mutations and neonatal cat exposure in atopic dermatitis

Research output: Contribution to journalLetter

  • Jacob P Thyssen
  • Tarunveer S Ahluwalia
  • Lavinia Paternoster
  • Natalia Ballardini
  • Anna Bergstrom
  • Erik Melén
  • Bo Lund Krogsgaard Chawes
  • Jakob Stokholm
  • JO’B Hourihane
  • D O'Sullivan
  • Peter Bager
  • Mads Melbye
  • Mariona Bustamante
  • Maties Torrent
  • Ana Esplugues
  • Liesbeth Duijts
  • Chen Hu
  • Niels Elbert
  • SGMA Pasmans
  • Tamar Nijsten
  • Andrea von Berg
  • Marie Standl
  • Tamara Schikowski
  • Gunda Herberth
  • Joachim Heinrich
  • Young-Ae Lee
  • Ingo Marenholz
  • Susanne Lau
  • John A Curtin
  • Angela Simpson
  • Adnan Custovic
  • Craig E Pennell
  • Carol A Wang
  • Patrick G Holt
  • Hans Bisgaard
  • Klaus Bønnelykke
Original languageEnglish
Number of pages5
Early online date5 Feb 2020
DateAccepted/In press - 18 Nov 2019
DateE-pub ahead of print (current) - 5 Feb 2020


Atopic dermatitis (AD) is a prevalent inflammatory skin disease. Loss-of-function mutations in filaggrin gene (FLG) represent the strongest genetic risk factors for AD, being strongly associated with early disease onset and persistence into adulthood.1 The epidermis of individuals with mutations in FLG is fundamentally different from normal skin being characterized by increased penetration of allergens.2

Recent birth cohort studies showed a significant interaction between cat ownership at birth and mutations in FLG (R501X, 2282del4) on the development of early-onset AD.3 This finding was replicated for the 2282del4 FLG mutation in a Dutch cohort study, and extended to further associate with risk of allergic sensitization.4 We performed analyses in multiple birth cohorts to examine the consistency and overall strength of the previously observed interaction.



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    Embargo ends: 5/02/21

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