Lembo, Serena (2010) IL-33 and keratinocytes: a trait d'union in innate immunity mechanisms of psoriasis. [Tesi di dottorato] (Inedito)

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Tipologia del documento: Tesi di dottorato
Lingua: English
Titolo: IL-33 and keratinocytes: a trait d'union in innate immunity mechanisms of psoriasis.
Autori:
AutoreEmail
Lembo, Serenaserenalembo@yahoo.it
Data: 29 Novembre 2010
Numero di pagine: 29
Istituzione: Università degli Studi di Napoli Federico II
Dipartimento: Patologia sistematica
Scuola di dottorato: Medicina clinica e sperimentale
Dottorato: Fisiopatologia clinica e medicina sperimentale
Ciclo di dottorato: 23
Coordinatore del Corso di dottorato:
nomeemail
Marone, Gianni[non definito]
Tutor:
nomeemail
Ayala, Fabioayala@unina.it
Data: 29 Novembre 2010
Numero di pagine: 29
Parole chiave: Psoriasis, interleukin-33 (IL-33), immunity
Settori scientifico-disciplinari del MIUR: Area 06 - Scienze mediche > MED/35 - Malattie cutanee e veneree
Informazioni aggiuntive: Per autorizzazione ricevuta dal Colleggio dei Docenti del Dottorato di Ricerca in Fisiopatologia Clinica e Medicina Sperimentale (XIII Ciclo), deposito la tesi in lingua inglese.
Depositato il: 02 Dic 2010 12:16
Ultima modifica: 30 Apr 2014 19:45
URI: http://www.fedoa.unina.it/id/eprint/8246

Abstract

IL-33 is a pro-inflammatory cytokine recently identified as a ligand for the orphan receptor ST2. IL-33 constitutive nuclear expression has been found in cells of tissues exposed to the environment. Moreover endothelial cells have been shown to abundantly express IL-33. Many of the inflammatory effects of IL-33 define its ability to induce Th2-type mediated responses but recently IL-33 was found to have a pro-inflammatory role in arthritis, which is Th1 and/or Th17 mediated. It can be hypothesized that IL-33 has a pro-inflammatory role in psoriasis too. In the present study we aimed to assess the role of IL-33 in psoriasis, investigating its property to promote inflammation via MC and KC activation. Here we report that IL-33 is elevated in the skin of psoriasis patients. Furthermore, IL-33 upregulates IL-4 and IL-13 and is able to induce a higher increase of MCP-1 and VEGF respect to TNF-α in MCs. In presence of TNF-α, IL-33 induces MCP-1 and IL-6, whereas in association with IL-17, is able to induce IL-20 in KCs. In conclusion, our study provides evidence that IL-33 is involved in psoriasis biology. Furthermore, our results reinforce the IL-33 activity in driving Th1 response too, contributing to the maintenance of psoriasis pathogenesis.

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