Mastrovito, Paola (2014) LRRFIP1 negatively regulates IL-17 signalling by binding to CIKS. [Tesi di dottorato]
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| Item Type: | Tesi di dottorato |
|---|---|
| Resource language: | English |
| Title: | LRRFIP1 negatively regulates IL-17 signalling by binding to CIKS |
| Creators: | Creators Email Mastrovito, Paola paola.mastrovito@gmail.com |
| Date: | 31 March 2014 |
| Number of Pages: | 55 |
| Institution: | Università degli Studi di Napoli Federico II |
| Department: | Medicina Molecolare e Biotecnologie Mediche |
| Scuola di dottorato: | Medicina molecolare |
| Dottorato: | Patologia e fisiopatologia molecolare |
| Ciclo di dottorato: | 26 |
| Coordinatore del Corso di dottorato: | nome email Avvedimento, Vittorio Enrico vittorioenrico.avvedimento@unina.it |
| Tutor: | nome email Leonardi, Antonio UNSPECIFIED |
| Date: | 31 March 2014 |
| Number of Pages: | 55 |
| Keywords: | LRRFIP1 isoform 3;IL-17;CIKS |
| Settori scientifico-disciplinari del MIUR: | Area 06 - Scienze mediche > MED/04 - Patologia generale |
| Date Deposited: | 10 Apr 2014 13:25 |
| Last Modified: | 15 Jul 2015 01:02 |
| URI: | http://www.fedoa.unina.it/id/eprint/9975 |
Collection description
Interleukin-17 (IL-17), the signature cytokine produced by T helper 17 (Th17) cells, plays crucial roles in host defense against microbial organisms and in the development of inflammatory diseases. IL-17 promotes the expression of cytokines and proteins involved in inflammatory responses, via the induction of gene transcription and post-transcription stabilization of mRNA. These functions are mediated by CIKS, an adaptor protein that is recruited to the receptor after IL-17 stimulation. We shows here that LRRFIP1 isoform 3 is a new CIKS interactor. Overexpression of LRRFIP1 isoform 3 blocks the IL-17 induced gene expression, via down-regulation of NF-κB and AP-1. Accordingly, down-regulation of LRRFIP1 enhanced the expression of cxcl1 and il-6 after IL-17 stimulation. LRRFIP 1 isoform 3 exerts this function by interfering with the recruitment of CIKS to the cytoplasmic domain of the IL-17 receptor. Collectively our finding defines a new mechanism regulating the inflammatory response.
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