國家衛生研究院 NHRI:Item 3990099045/12620
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    題名: Interleukin 26 skews macrophage polarization towards M1 phenotype by activating cJUN and the NF-kappaB pathway
    其他題名: Interleukin 26 skews macrophage polarization towards M1 phenotype by activating cJUN and the NF-κB pathway
    作者: Lin, YH;Wang, YH;Peng, YJ;Liu, FC;Lin, GJ;Huang, SH;Sytwu, HK;Cheng, CP
    貢獻者: National Institute of Infectious Diseases and Vaccinology
    摘要: Interleukin 26 (IL-26) is a new member of the IL-10 family that is highly expressed in rheumatoid arthritis (RA). However, the functions of IL-26 produced by macrophages in RA have not been elucidated. In the present work, we evaluated the effects and the mechanisms of IL-26 on M1 and M2 macrophage differentiation. Human or mouse macrophage cells were treated with lipopolysaccharides (LPS), interferon gamma (IFNgamma), or IL-4 alone or concurrently treated with IL-26 to monitor M1 or M2 macrophage subtypes. The expression level of M1 or M2 macrophage genes was evaluated by reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). The molecular mechanisms of downstream signaling activation during differentiation were investigated by immunoblotting assay. Our results found that IL-26 promoted macrophage cells from CD80(+) M1 macrophage differentiation, not from the CD206(+) M2 phenotype. The messenger RNA of M1-type macrophage markers tumor necrosis factor alpha (TNFalpha) and inducible nitric oxide synthase (iNOS) was up-regulated in the IL-26-treated group. Also, the M1-related proinflammatory cytokines TNFalpha and IL-6 were induced after IL-26 stimulation. Interestingly, IL-10, a cytokine marker of M2 macrophage, was also elevated after IL-26 stimulation. Moreover, the M1-like macrophage stimulated by IL-26 underwent cJUN, nuclear factor kappa B (NF-kappaB), and signal transducer and activator of transcription 1 (STAT1) activation. Our findings suggested the role of IL-26 in synovial macrophages of active rheumatoid arthritis and provided a new insight into IL-26 as a candidate therapeutic target in rheumatoid arthritis.
    日期: 2020-04-10
    關聯: Cells. 2020 Apr 10;9(4):Article number 938.
    Link to: http://dx.doi.org/10.3390/cells9040938
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=2073-4409&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000535559500149
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85083412388
    顯示於類別:[司徒惠康] 期刊論文

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