Accumulation and activation of epidermal γδ T cells in a mouse model of chronic dermatitis is not required for the inflammatory phenotype.
Eur J Immunol
; 45(9): 2517-28, 2015 Sep.
Article
en En
| MEDLINE
| ID: mdl-26081170
Chronic skin inflammation resulting from a defective epidermal barrier is a hallmark of atopic dermatitis (AD). We previously demonstrated that mice lacking FGF receptors 1 and 2 in keratinocytes (K5-R1/R2 mice) develop an AD-like chronic dermatitis as a result of an impaired epidermal barrier. Here, we show that γδ T cells, which rapidly respond to various insults, accumulate in the epidermis of K5-R1/R2 mice before the development of histological abnormalities. Their number and activation further increase as the phenotype progresses, most likely as a consequence of increased expression of Il-2 and Il-7 and the stress-induced proteins Rae-1, H60c, Mult1, PlexinB2, and Skint1. To determine the role of γδ T cells in the skin phenotype, we generated quadruple mutant K5-R1/-R2 mice lacking γδ T cells. Surprisingly, loss of γδ T cells did not or only marginally affect keratinocyte proliferation, epidermal thickness, epidermal barrier function, and accumulation and activation of different immune cells in the skin of K5-R1/R2 mice, possibly due to partial compensation by αß T cells. These results demonstrate that γδ T cells do not contribute to the development or maintenance of chronic inflammation in response to a defect in the epidermal barrier.
Palabras clave
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Queratinocitos
/
Subgrupos de Linfocitos T
/
Receptores de Antígenos de Linfocitos T gamma-delta
/
Dermatitis
/
Receptor Tipo 1 de Factor de Crecimiento de Fibroblastos
/
Receptor Tipo 2 de Factor de Crecimiento de Fibroblastos
Tipo de estudio:
Prognostic_studies
Idioma:
En
Revista:
Eur J Immunol
Año:
2015
Tipo del documento:
Article
País de afiliación:
Suiza
Pais de publicación:
Alemania