Mastrovito, Paola
(2014)
LRRFIP1 negatively regulates IL-17 signalling by binding to
CIKS.
[Tesi di dottorato]
| 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 |
[error in script]
[error in script]
| 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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