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Spontaneous atopic dermatitis is mediated by innate immunity, with the secondary lung inflammation of the atopic march requiring adaptive immunity.
Saunders, Sean P; Moran, Tara; Floudas, Achilleas; Wurlod, Felicity; Kaszlikowska, Agnieszka; Salimi, Maryam; Quinn, Emma M; Oliphant, Christopher J; Núñez, Gabriel; McManus, Ross; Hams, Emily; Irvine, Alan D; McKenzie, Andrew N J; Ogg, Graham S; Fallon, Padraic G.
Afiliación
  • Saunders SP; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
  • Moran T; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
  • Floudas A; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
  • Wurlod F; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
  • Kaszlikowska A; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
  • Salimi M; MRC Human Immunology Unit, NIHR Biomedical Research Centre, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
  • Quinn EM; Institute of Molecular Medicine, St James's Hospital, Dublin, Ireland.
  • Oliphant CJ; MRC Laboratory of Molecular Biology, Cambridge, United Kingdom; Biosceptre, Babraham Research Campus, Babraham, Cambridge, United Kingdom.
  • Núñez G; Department of Pathology and Comprehensive Cancer Center, University of Michigan, Ann Arbor, Mich.
  • McManus R; Institute of Molecular Medicine, St James's Hospital, Dublin, Ireland.
  • Hams E; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland.
  • Irvine AD; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland; Department of Paediatric Dermatology, Our Lady's Children's Hospital, Dublin, Ireland.
  • McKenzie AN; MRC Laboratory of Molecular Biology, Cambridge, United Kingdom.
  • Ogg GS; MRC Human Immunology Unit, NIHR Biomedical Research Centre, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom.
  • Fallon PG; Trinity Biomedical Sciences Institute, Trinity College Dublin, Dublin, Ireland; National Children's Research Centre, Our Lady's Children's Hospital, Dublin, Ireland; Institute of Molecular Medicine, St James's Hospital, Dublin, Ireland. Electronic address: pfallon@tcd.ie.
J Allergy Clin Immunol ; 137(2): 482-91, 2016 Feb.
Article en En | MEDLINE | ID: mdl-26299987
BACKGROUND: Atopic dermatitis (AD) is an inflammatory skin condition that can occur in early life, predisposing to asthma development in a phenomenon known as the atopic march. Although genetic and environmental factors are known to contribute to AD and asthma, the mechanisms underlying the atopic march remain poorly understood. Filaggrin loss-of-function mutations are a major genetic predisposer for the development of AD and progression to AD-associated asthma. OBJECTIVE: We sought to experimentally address whether filaggrin mutations in mice lead to the development of spontaneous eczematous inflammation and address the aberrant immunologic milieu arising in a mouse model of filaggrin deficiency. METHODS: Filaggrin mutant mice were generated on the proallergic BALB/c background, creating a novel model for the assessment of spontaneous AD-like inflammation. Independently recruited AD case collections were analyzed to define associations between filaggrin mutations and immunologic phenotypes. RESULTS: Filaggrin-deficient mice on a BALB/c background had profound spontaneous AD-like inflammation with progression to compromised pulmonary function with age, reflecting the atopic march in patients with AD. Strikingly, skin inflammation occurs independently of adaptive immunity and is associated with cutaneous expansion of IL-5-producing type 2 innate lymphoid cells. Furthermore, subjects with filaggrin mutations have an increased frequency of type 2 innate lymphoid cells in the skin in comparison with control subjects. CONCLUSION: This study provides new insights into our understanding of the atopic march, with innate immunity initiating dermatitis and the adaptive immunity required for subsequent development of compromised lung function.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neumonía / Dermatitis Atópica / Inmunidad Adaptativa / Inmunidad Innata Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Allergy Clin Immunol Año: 2016 Tipo del documento: Article País de afiliación: Irlanda Pais de publicación: Estados Unidos
Texto completo
Añadir a Mi BVS
Imprimir
XML
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Neumonía / Dermatitis Atópica / Inmunidad Adaptativa / Inmunidad Innata Tipo de estudio: Prognostic_studies Límite: Animals Idioma: En Revista: J Allergy Clin Immunol Año: 2016 Tipo del documento: Article País de afiliación: Irlanda Pais de publicación: Estados Unidos