immunology-2018-scientifictracks

Immunology 2018

J u l y 0 5 - 0 7 , 2 0 1 8

V i e n n a , A u s t r i a

Page 34

Journal of Clinical Immunology and Allergy

ISSN 2471-304X

1 5

t h

I n t e r n a t i o n a l C o n f e r e n c e o n

Immunology

roper control of immune responses by Foxp3

regulatory T cells at inflamed

sites is crucial for the prevention of immunopathology. TGF-β induced

Foxp3+ regulatory T (iTreg) cells are generated in inflammatory environments

as well as in steady state conditions. Inflammatory cytokines such as IFN-γ

and IL-4 have an antagonistic effect on iTreg cell conversion. However, it is

not known how naive CD4

T cells overcome the inhibitory environment in

inflamed sites to differentiate into iTreg cells. Here, we show that CCAAT/

Enhancer-binding protein (C/EBP) functions as a safeguard that enhances

iTreg generation by dampening the inhibitory effect of IFN-γ and IL-4 on Foxp3

expression. We found that C/EBPβ is induced by retinoic acid and binds to the

methyl-CRE sequence in the

Foxp3

TSDR to sustain its expression. C/EBPβ-

transduced iTreg cells showed more potent suppressive activity in mouse

disease models for experimental autoimmune encephalitis. We also found that

C/EBPβ-transduced human iTreg cells exhibited more enhanced suppressor

function in

in vitro

suppression assay. These results establish C/EBP as a new

molecular target for stabilizing iTreg cells in inflammatory environments.

Biography

Rho H Seong has completed his PhD from Stanford University

and Post-doctoral studies from Stanford University School of

Medicine. He is the Director of Institute of Molecular Biology

and Genetics, Seoul National University. He has published more

than 90 papers in reputed journals and has served as an Editor-

In-Chief of

Molecules and Cells.

Foxp3 expression in iTreg cells is stabilized by C/EBP in

inflammatory environments

Rho H Seong, Sung-Kyu Lee, Jieun Kim, Hyungyu Min and

Kyungsoo Park

Seoul National University, Korea

Rho H Seong et al., Insights Allergy Asthma Bronchitis 2018, Volume: 4

DOI: 10.21767/2471-304X-C1-002