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Autor(en) / Beteiligte
Titel
The IL‐13–OVOL1–FLG axis in atopic dermatitis
Ist Teil von
  • Immunology, 2019-12, Vol.158 (4), p.281-286
Ort / Verlag
England: Wiley Subscription Services, Inc
Erscheinungsjahr
2019
Quelle
Wiley-Blackwell Journals
Beschreibungen/Notizen
  • Summary Despite sharing interleukin‐4 receptor α (IL‐4Rα) in their signaling cascades, IL‐4 and IL‐13 have different functions in atopic inflammation. IL‐13 preferentially participates in the peripheral tissues because tissue‐resident group 2 innate lymphoid cells produce IL‐13 but not IL‐4. In contrast, lymph node T follicular helper cells express IL‐4 but not IL‐13 to regulate B‐cell immunity. The dominant microenvironment of IL‐13 is evident in the lesional skin of atopic dermatitis (AD). The IL‐13‐rich local milieu causes barrier dysfunction by down‐regulating the OVOL1–filaggrin (FLG) axis and up‐regulating the periostin–IL‐24 axis. Genome‐wide association studies also point to the crucial involvement of the IL‐13, OVOL1 and FLG genes in the pathogenesis of AD. Biologics targeting IL‐13, such as the anti‐IL‐4Rα antibody dupilumab and the anti‐IL‐13 antibody tralokinumab, successfully improve AD lesions and further highlight the importance of IL‐13 in the pathogenesis of AD. The dominant microenvironment of IL‐13 is evident in the lesional skin of atopic dermatitis. IL‐13 causes barrier dysfunction by down‐regulating the OVOL1–filaggrin axis. IL‐13 also induces barrier dysfunction by up‐regulating the periostin–IL‐24 axis.

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