BiopestPeptidV1, Main, Exploration, bibRecord, 000009

The psoriatic shift induced by interleukin 17 is promptly reverted by a specific anti-IL-17A agent in a three-dimensional organotypic model of normal human skin culture.

Identifieur interne : 000009 ( Main/Exploration ); précédent : 000008; suivant : 000010

The psoriatic shift induced by interleukin 17 is promptly reverted by a specific anti-IL-17A agent in a three-dimensional organotypic model of normal human skin culture.

Auteurs : Elena Donetti [Italie] ; Giulia Lombardo ; Serena Indino ; Laura Cornaghi ; Francesca Arnaboldi ; Leonardo Pescitelli ; Franz Baruffaldi Preis ; Francesca Prignano

Source :

European journal of histochemistry : EJH [ 2038-8306 ] ; 2020.

RBID : pubmed:32312032

Descripteurs français

KwdFr :
- Adulte (MeSH), Anticorps monoclonaux (immunologie), Anticorps monoclonaux (pharmacologie), Cellules de Langerhans (métabolisme), Femelle (MeSH), Humains (MeSH), Interleukine-17 (antagonistes et inhibiteurs), Interleukine-17 (immunologie), Interleukine-17 (pharmacologie), Jeune adulte (MeSH), Kératines (métabolisme), Occludine (métabolisme), Peau (métabolisme), Peau (ultrastructure), Protéines S100 (métabolisme), Psoriasis (anatomopathologie), Psoriasis (métabolisme), Récepteur de type Toll-4 (métabolisme), Sous-unité p50 de NF-kappa B (métabolisme).
MESH :
- anatomopathologie : Psoriasis.
- antagonistes et inhibiteurs : Interleukine-17.
- immunologie : Anticorps monoclonaux, Interleukine-17.
- métabolisme : Cellules de Langerhans, Kératines, Occludine, Peau, Protéines S100, Psoriasis, Récepteur de type Toll-4, Sous-unité p50 de NF-kappa B.
- pharmacologie : Anticorps monoclonaux, Interleukine-17.
- ultrastructure : Adulte, Femelle, Humains, Jeune adulte, Peau.

English descriptors

KwdEn :
- Adult (MeSH), Antibodies, Monoclonal (immunology), Antibodies, Monoclonal (pharmacology), Female (MeSH), Humans (MeSH), Interleukin-17 (antagonists & inhibitors), Interleukin-17 (immunology), Interleukin-17 (pharmacology), Keratins (metabolism), Langerhans Cells (metabolism), NF-kappa B p50 Subunit (metabolism), Occludin (metabolism), Psoriasis (metabolism), Psoriasis (pathology), S100 Proteins (metabolism), Skin (metabolism), Skin (ultrastructure), Toll-Like Receptor 4 (metabolism), Young Adult (MeSH).
MESH :
- chemical , antagonists & inhibitors : Interleukin-17.
- chemical , immunology : Antibodies, Monoclonal, Interleukin-17.
- chemical , metabolism : Keratins, NF-kappa B p50 Subunit, Occludin, S100 Proteins, Toll-Like Receptor 4.
- chemical , pharmacology : Antibodies, Monoclonal, Interleukin-17.
- metabolism : Langerhans Cells, Psoriasis, Skin.
- pathology : Psoriasis.
- ultrastructure : Skin.
- Adult, Female, Humans, Young Adult.

Abstract

Interleukin 17A (IL-17A), mainly produced by the T helper subclass Th17, plays a key role in the psoriatic plaque formation and progression. The clinical effectiveness of anti-IL-17A agents is documented, but the early and specific mechanisms of their protection are not identified yet. The challenge of the present study is to investigate the possible reversal exerted by a specific anti-IL-17A agent on the psoriatic events induced by IL-17A in a three-dimensional organotypic model of normal human skin. Bioptic skin fragments obtained after aesthetic surgery of healthy women (n=5) were incubated with i) IL-17A biological inhibitor (anti-IL-17A), ii) IL-17A, iii) a combination of IL-17A and its specific IL-17A biological inhibitor (COMBO). A Control group was in parallel cultured and incubation lasted for 24 and 48 h epidermal-side-up at the air-liquid interface. All subjects were represented in all experimental groups at all considered time-points. Keratinocyte proliferation and the presence of epidermal Langerhans cells were quantitatively estimated. In parallel with transmission electron microscopy analysis, immunofluorescence studies for the epidermal distribution of keratin (K)10, K14, K16, K17, filaggrin/occludin, Toll-like Receptor 4, and Nuclear Factor kB were performed. IL-17A inhibited cell proliferation and induced K17 expression, while samples incubated with the anti-IL-17A agent were comparable to controls. In the COMBO group the IL-17A-induced effects were almost completely reverted. Our study, for the first time, elucidates the most specific psoriatic cellular events that can be partially affected or completely reverted by a specific anti-IL-17A agent during the early phases of the plaque onset and progression. On the whole, this work contributes to expand the knowledge of the psoriatic tableau.

DOI: 10.4081/ejh.2020.3115
PubMed: 32312032
PubMed Central: PMC7171424

Affiliations:

Italie

Links toward previous steps (curation, corpus...)

to stream Main, to step Corpus: 000059
to stream Main, to step Curation: 000059

Le document en format XML

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<term>Anticorps monoclonaux (pharmacologie)</term>
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<term>Interleukine-17 (immunologie)</term>
<term>Interleukine-17 (pharmacologie)</term>
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<front><div type="abstract" xml:lang="en">Interleukin 17A (IL-17A), mainly produced by the T helper subclass Th17, plays a key role in the psoriatic plaque formation and progression. The clinical effectiveness of anti-IL-17A agents is documented, but the early and specific mechanisms of their protection are not identified yet. The challenge of the present study is to investigate the possible reversal exerted by a specific anti-IL-17A agent on the psoriatic events induced by IL-17A in a three-dimensional organotypic model of normal human skin. Bioptic skin fragments obtained after aesthetic surgery of healthy women (n=5) were incubated with i) IL-17A biological inhibitor (anti-IL-17A), ii) IL-17A, iii) a combination of IL-17A and its specific IL-17A biological inhibitor (COMBO). A Control group was in parallel cultured and incubation lasted for 24 and 48 h epidermal-side-up at the air-liquid interface. All subjects were represented in all experimental groups at all considered time-points. Keratinocyte proliferation and the presence of epidermal Langerhans cells were quantitatively estimated. In parallel with transmission electron microscopy analysis, immunofluorescence studies for the epidermal distribution of keratin (K)10, K14, K16, K17, filaggrin/occludin, Toll-like Receptor 4, and Nuclear Factor kB were performed. IL-17A inhibited cell proliferation and induced K17 expression, while samples incubated with the anti-IL-17A agent were comparable to controls. In the COMBO group the IL-17A-induced effects were almost completely reverted. Our study, for the first time, elucidates the most specific psoriatic cellular events that can be partially affected or completely reverted by a specific anti-IL-17A agent during the early phases of the plaque onset and progression. On the whole, this work contributes to expand the knowledge of the psoriatic tableau.</div>
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<Abstract><AbstractText>Interleukin 17A (IL-17A), mainly produced by the T helper subclass Th17, plays a key role in the psoriatic plaque formation and progression. The clinical effectiveness of anti-IL-17A agents is documented, but the early and specific mechanisms of their protection are not identified yet. The challenge of the present study is to investigate the possible reversal exerted by a specific anti-IL-17A agent on the psoriatic events induced by IL-17A in a three-dimensional organotypic model of normal human skin. Bioptic skin fragments obtained after aesthetic surgery of healthy women (n=5) were incubated with i) IL-17A biological inhibitor (anti-IL-17A), ii) IL-17A, iii) a combination of IL-17A and its specific IL-17A biological inhibitor (COMBO). A Control group was in parallel cultured and incubation lasted for 24 and 48 h epidermal-side-up at the air-liquid interface. All subjects were represented in all experimental groups at all considered time-points. Keratinocyte proliferation and the presence of epidermal Langerhans cells were quantitatively estimated. In parallel with transmission electron microscopy analysis, immunofluorescence studies for the epidermal distribution of keratin (K)10, K14, K16, K17, filaggrin/occludin, Toll-like Receptor 4, and Nuclear Factor kB were performed. IL-17A inhibited cell proliferation and induced K17 expression, while samples incubated with the anti-IL-17A agent were comparable to controls. In the COMBO group the IL-17A-induced effects were almost completely reverted. Our study, for the first time, elucidates the most specific psoriatic cellular events that can be partially affected or completely reverted by a specific anti-IL-17A agent during the early phases of the plaque onset and progression. On the whole, this work contributes to expand the knowledge of the psoriatic tableau.</AbstractText>
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The psoriatic shift induced by interleukin 17 is promptly reverted by a specific anti-IL-17A agent in a three-dimensional organotypic model of normal human skin culture.

The psoriatic shift induced by interleukin 17 is promptly reverted by a specific anti-IL-17A agent in a three-dimensional organotypic model of normal human skin culture.

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