In:
Experimental Dermatology, Wiley, Vol. 25, No. 4 ( 2016-04), p. 311-313
Abstract:
T‐cells expressing α E ( CD 103), an integrin induced by TGF β on T‐cells in vitro , accumulate within epithelia in inflammatory disorders, including psoriasis. However, it is unclear, if and how α E ( CD 103) contributes to skin inflammation. Using two complementary approaches, we have investigated α E ( CD 103) in psoriasis‐like skin inflammation of mice with transgenic epidermal expression of human TGF β1: α E ( CD 103) was inhibited by function‐blocking antibodies in vivo, and double‐mutants with additional α E ( CD 103)‐depletion were generated in two different genetic backgrounds. Epidermal h TGF β1 expression was associated with prominent expression of α E ( CD 103) on infiltrating cells. However, neither treatment with α E ( CD 103)‐blocking antibodies nor deficiency of α E ( CD 103) in double‐mutant mice altered the psoriasis‐like phenotype. In addition, histopathological and flow cytometric analyses revealed similar pathological skin alterations and lymphocyte subgroups in the different mouse strains. Thus, while α E ( CD 103) expression is indeed associated with h TGF β1 in vivo , it has little, if any, influence on the course of the psoriasis‐like phenotype in K5.h TGF β1 transgenic mice.
Type of Medium:
Online Resource
ISSN:
0906-6705
,
1600-0625
DOI:
10.1111/exd.2016.25.issue-4
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
2026228-0
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