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Journal of Clinical Immunology

Erschienen in:

01.03.2010

Interleukin-32γ Enhances the Production of IL-6 and IL-8 in Fibroblast-Like Synoviocytes Via Erk1/2 Activation

verfasst von: Yong-Gil Kim, Chang-Keun Lee, Soo-Hyun Kim, Woo-Shin Cho, Se Hwan Mun, Bin Yoo

Erschienen in: Journal of Clinical Immunology | Ausgabe 2/2010

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Abstract

Introduction

In the present study, we examined the effect of the pro-inflammatory cytokine IL-32γ, the most biologically active isoform, and its related molecules in fibroblast-like synoviocytes (FLS).

Materials and Methods

FLS were isolated from synovial tissues of rheumatoid arthritis (RA) patients. The secretion and expression of IL-6 and IL-8 were examined by ELISA and real-time PCR, and the activation of signaling molecules was evaluated by Western blot, electrophoretic mobility shift assay (EMSA), real-time PCR, and siRNA transfection.

Results

By IL-32γ stimulation in RA FLS, the expressions of IL-6 and IL-8 were increased significantly, and the phosphorylated Erk1/2 and AP-1 were expressed prominently in Western blot and EMSA. In the Erk1/2 inhibited cells, IL-32γ stimulation did not increase the mRNA expression of IL-6 and IL-8.

Conclusion

Our results suggest that IL-32γ stimulation can induce the production of IL-6 and IL-8 from RA FLS via Erk1/2 activation.

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Titel: Interleukin-32γ Enhances the Production of IL-6 and IL-8 in Fibroblast-Like Synoviocytes Via Erk1/2 Activation
verfasst von: Yong-Gil Kim
Chang-Keun Lee
Soo-Hyun Kim
Woo-Shin Cho
Se Hwan Mun
Bin Yoo
Publikationsdatum: 01.03.2010
Verlag: Springer US
Erschienen in: Journal of Clinical Immunology / Ausgabe 2/2010
Print ISSN: 0271-9142
Elektronische ISSN: 1573-2592
DOI: https://doi.org/10.1007/s10875-009-9360-2

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Interleukin-32γ Enhances the Production of IL-6 and IL-8 in Fibroblast-Like Synoviocytes Via Erk1/2 Activation

Abstract

Introduction

Materials and Methods

Results

Conclusion

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Live-Webinar: Aktuelle Leitlinien bei Herz-Kreislauf-Erkrankungen

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Abstract

Introduction

Materials and Methods

Results

Conclusion

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