Cimaz, R

Corinaldesi, E

de Martino, M

Fanti, F

Giani, T

Olivito, B

Simonini, G

English

PubMed

G Simonini

B Olivito

F Fanti

T Giani

E Corinaldesi

M de Martino

R Cimaz

Springer - Publisher Connector

FOXP3 Polymorphism and gene expression in Italian patients with Kawasaki Syndrome

BioMed Central
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Pediatric Rheumatology
Open AccessPoster presentation
FOXP3 Polymorphism and gene expression in Italian patients with 
Kawasaki Syndrome
G Simonini*, B Olivito, F Fanti, T Giani, E Corinaldesi, M de Martino and 
R Cimaz
Address: Rheumatology Unit-Dept. of Pediatrics, University of Florence, Firenze, Italy
* Corresponding author    
Background
The transcription factor FOXP3 is a key regulator of
immune homeostasis of natural regulatory T lymphocytes
(Treg). Aim of our study was to investigate the link
between the FOXP3 gene expression and polymorphism,
and Kawasaki Syndrome (KS).
Materials and methods
The single nucleotide polymorphism (SNP) at position
543 of exon 5 of FOXP3 was investigated in 58 caucasian
children patients with KS (F:30, M:28), recruited at our
Paediatric Reumatology Unit. In 6 patients we could eval-
uate the percentage of circulating CD4+ T cells co-express-
ing CD25 and FOXP3 by flow cytometry, mRNA
transcripts of FOXP3 in PBMCs by Real Time PCR (with
Rnase P as internal control gene), and the levels of IL-17
in PBMCs supernatants (5 × 104 cells) by a quantitative
immunoassay Kit.
Results
In KS subject, 2 females (3.4%) showed the 543 SNP in
heterozygosis (C>T), as actually reported in healthy euro-
pean females (4.3%). FOXP3 mRNA expression was sig-
nificantly lower (3-fold) than in healthy controls, while
FOXP3 protein expression determined by flow cytometry
was not lower than in controls. IL-17 levels were 8-fold
higher in KS than in controls (mean 340 vs 40 pg/mL)
Conclusion
Compared to healthy controls, in our patients, FOXP3
gene 543 SNP does not differ, FOXP3 mRNA expression
was lower, without a correspondent lower protein expres-
sion, and IL-17 levels were much higher in patients. Due
to the small number of patients, these results warrant fur-
ther studies to evaluate FOXP3 expression in relationship
with IL-17 in KS.
from 15th Paediatric Rheumatology European Society (PreS) Congress
London, UK. 14–17 September 2008
Published: 15 September 2008
Pediatric Rheumatology 2008, 6(Suppl 1):P259 doi:10.1186/1546-0096-6-S1-P259
<supplement> <title> <p>15<sup>th </sup>Paediatric Rheumatology European Society (PreS) Congress</p> </title> <editor>Wietse Kuis, Patricia Woo, Angelo Ravelli, Hermann Girschick, Michaël Hofer, Johannes Roth, Rotraud K Saurenmann, Alberto Martini, Pavla Dolezova, Janjaap van der Net, Pierre Quartier, Lucy Wedderburn and Jan Scott</editor> <note>Meeting abstracts – A single PDF containing all abstracts in this Supplement is available <a href="http://www.biomedcentral.com/content/files/PDF/1546-0096-6-S1-full.pdf">here</a>.</note> </supplement>
This abstract is available from: http://www.ped-rheum.com/content/6/S1/P259
© 2008 Simonini et al; licensee BioMed Central Ltd. 


Simonini G

Olivito B

Fanti F

Giani T

Corinaldesi E

de Martino M

Cimaz R

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FOXP3 Polymorphism and gene expression in Italian patients with Kawasaki Syndrome

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