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Migita, K. et al.

K. Migita, T. Koga, T. Torigoshi, S. Motokawa, Y. Maeda, Y. Jiuchi, Y. Izumi, T. Miyashita, M. Nakamura, A. Komori, H. Ishibashi,

Induction of interleukin-23 p19 by serum amyloid A (SAA) in rheumatoid synoviocytes.

In this study, we investigated the roles of serum amyloid A (SAA) in T helper 17 (Th17)-related cytokine induction in rheumatoid arthritis (RA) synoviocytes. Synoviocytes isolated from rheumatoid arthritis (RA) patients were stimulated with recombinant SAA and IL-23 expression was investigated using reverse transcriptase-polymerase chain reaction and Western blot. The involvement of mitogen-activated protein kineases (MAPKs) and nuclear factor (NF)-κB in SAA-induced interleukin (IL)-23 p19 expression was investigated using pharmacological inhibitors. In RA synoviocytes, SAA induced the expression of IL-23 p19 and p40 mRNA expression. The SAA-stimulated expression of p19 was rapid (< 3 h), and insensitive to polymyxin B treatment. This SAA-stimulated expression of IL-23 p19 was inhibited completely by inhibitors of NF-κB, p38MAPK and dexamethasone. Interestingly, the SAA-induced IL-23, p19 and p40 production was accompanied by enhanced expression of IL-1β, but not transforming growth factor-β. These results indicate that SAA is a significant inducer of IL-23 and IL-1β in RA synoviocytes and potentially activates the IL-23/IL-17 pathway in the RA synovium. Our data present a novel interaction between inflammation and autoimmunity by an acute-phase protein.[1]

References

Induction of interleukin-23 p19 by serum amyloid A (SAA) in rheumatoid synoviocytes. Migita, K., Koga, T., Torigoshi, T., Motokawa, S., Maeda, Y., Jiuchi, Y., Izumi, Y., Miyashita, T., Nakamura, M., Komori, A., Ishibashi, H. Clin. Exp. Immunol. (2010) [Pubmed]

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