Th2 Cytokines Affect the Innate Immune Barrier without Impairing the Physical Barrier in a 3D Model of Normal Human Skin
Articolo
Data di Pubblicazione:
2023
Citazione:
Th2 Cytokines Affect the Innate Immune Barrier without Impairing the Physical Barrier in a 3D Model of Normal Human Skin / E.B. Donetti, F. Riva, S.L. Indino, G. Lombardo, F. Baruffaldi Preis, E. Rosi, F. Prignano. - In: JOURNAL OF CLINICAL MEDICINE. - ISSN 2077-0383. - 12:5(2023 Mar), pp. 1941.1-1941.19. [10.3390/jcm12051941]
Abstract:
Background: Atopic dermatitis is one of the most common inflammatory skin diseases characterized by T helper (Th) 2 and Th22 cells producing interleukin (IL)-4/IL-13 and IL-22, respectively. The specific contribution of each cytokine to the impairment of the physical and the immune barrier via Toll-like receptors (TLRs) is poorly addressed concerning the epidermal compartment of the skin. (2) Methods: The effect of IL-4, IL-13, IL-22, and the master cytokine IL-23 is evaluated in a 3D model of normal human skin biopsies (n = 7) at the air-liquid interface for 24 and 48 h. We investigated by immunofluorescence the expressions of (i) claudin-1, zonula occludens (ZO)-1 filaggrin, involucrin for the physical barrier and (ii) TLR2, 4, 7, 9, human beta-defensin 2 (hBD-2) for the immune barrier. (3) Results: Th2 cytokines induce spongiosis and fail in impairing tight junction composition, while IL-22 reduces and IL-23 induces claudin-1 expression. IL-4 and IL-13 affect the TLR-mediated barrier largely than IL-22 and IL-23. IL-4 early inhibits hBD-2 expression, while IL-22 and IL-23 induce its distribution. (4) Conclusions: This experimental approach looks to the pathogenesis of AD through molecular epidermal proteins rather than cytokines only and paves the way for tailored patient therapy.
Tipologia IRIS:
01 - Articolo su periodico
Keywords:
claudin-1; filaggrin; human beta-defensin 2; human epidermis; immunofluorescence; interleukins; involucrin; keratinocytes; toll-like receptors; transmission electron microscopy;
Elenco autori:
E. Donetti, F. Riva, S. Indino, G. Lombardo, F. Baruffaldi Preis, E. Rosi, F. Prignano
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