alexa Opposing Roles Of TGF-β In Prostaglandin Production By Human Follicular Dendritic Cell-like Cells
ISSN: 1745-7580

Immunome Research
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8th Molecular Immunology and Immunogenetics Congress
March 20-21, 2017 Rome, Italy

Jongseon Choe and Jihoon Park
Kangwon National University, South Korea
Posters & Accepted Abstracts: J Immunome Res
DOI: 10.4172/1745-7580.C1.012
Abstract
Prostaglandins (PGs) are recognized as important immune regulators. Using human follicular dendritic cell (FDC)-like HK cells, we have investigated the immunoregulatory role of PGs and their production mechanisms. The present study was aimed at determining the role of TGF-β in IL-1β-induced cyclooxygenase-2 (COX-2) expression by immuno-blotting. COX-2 is the key enzyme responsible for PG production in HK cells. TGF-β, when added simultaneously with IL-1β, gave an additive effect on COX- 2 expression in a dose-dependent manner. However, TGF-β inhibited IL-1β-stimulated COX-2 expression when it was added at least 12 hours before IL-1β addition. The inhibitory effect of TGF-β was specific to IL-1β-induced COX-2 expression in HK cells. The stimulating and inhibitory effects of TGF-β were reproduced in IL-1β-stimulated PG production. Based on our previous results of the essential requirement of ERK and p38 MAPKs in TGF-β-induced COX-2 expression, we examined whether the differential activation of these MAPKs would underlie the opposing activities of TGF-β. The phosphorylation of ERK and p38 MAPKs was indeed enhanced or suppressed by the simultaneous treatment or pre-treatment, respectively. These results suggest that TGF-β exerts opposing effects on IL-1β-induced COX-2 expression in HK cells by differentially regulating activation of ERK and p38 MAPKs.
Biography

Jongseon Choe is leading the Laboratory of Cellular Immunobiology at Kangwon National University, trying to understand how our body defends against the various pathogenic microorganisms. His team is currently focusing on the pivotal branch of the immune system, the humoral immune response.

Email: [email protected]

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