Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

BACKGROUND: Filaggrin null mutations associate with atopic eczema and also with asthma when present with eczema. However, while epidermal dysfunction is an important factor in disease pathogenesis, it is unclear how such dysfunction interacts with immune responses to contribute to cutaneous and other inflammatory atopic disease. OBJECTIVES: To gain a better understanding of the mechanisms underlying such predisposition in order to understand different disease phenotypes and possibly identify potential treatment targets. METHODS: We studied 33 individuals with atopic eczema and used interleukin-4 immunospot and human leucocyte antigen class II tetrameric complexes to investigate the peripheral blood allergen-specific CD4+ T-cell responses. RESULTS: Filaggrin null mutations associated with significantly (P<0·05) higher frequencies of allergen-specific CD4+ T-helper 2 cell responses. CONCLUSIONS: These data would support a model where barrier dysfunction possibly promotes greater allergen penetration and delivery to drive allergen-specific CD4+ T cells. This could further contribute to respiratory and cutaneous inflammatory disease.

Original publication

DOI

10.1111/j.1365-2133.2010.09866.x

Type

Journal article

Journal

Br J Dermatol

Publication Date

09/2010

Volume

163

Pages

544 - 549

Keywords

Adult, CD4-Positive T-Lymphocytes, Eczema, Genetic Predisposition to Disease, HLA Antigens, Humans, Immunity, Cellular, Interleukin-4, Intermediate Filament Proteins, Phenotype, Polymerase Chain Reaction, T-Lymphocytes, Helper-Inducer