抄録
Whereas interleukin-6 (IL-6) is a proinflammatory cytokine, IL-10 is an anti-inflammatory cytokine. Although signal transducer and activator of transcription 3 (STAT3) is essential for the function of both IL-6 and IL-10, it is unclear how these two cytokines have such opposing functions. Here we show that suppressor of cytokine signaling 3 (SOCS3) is a key regulator of the divergent action of these two cytokines. In macrophages lacking the Socs3 gene or carrying a mutation of the SOCS3-binding site in gp130, the lipopolysaccharide-induced production of tumor necrosis factor (TNF) and IL-12 is suppressed by both IL-10 and IL-6. SOCS3 specifically prevents activation of STAT3 by IL-6 but not IL-10. Taken together, these data indicate that SOCS3 selectively blocks signaling by IL-6, thereby preventing its ability to inhibit LPS signaling.
| 元の言語 | English |
|---|---|
| ページ（範囲） | 551-556 |
| ページ数 | 6 |
| ジャーナル | Nature Immunology |
| 巻 | 4 |
| 発行部数 | 6 |
| DOI | |
| 出版物ステータス | Published - 2003 6 1 |
| 外部発表 | Yes |
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ASJC Scopus subject areas
- Immunology
これを引用
IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages. / Yasukawa, Hideo; Ohishi, Masanobu; Mori, Hiroyuki; Murakami, Masaaki; Chinen, Takatoshi; Aki, Daisuke; Hanada, Toshikatsu; Takeda, Kiyoshi; Akira, Shizuo; Hoshijima, Masahiko; Hirano, Toshio; Chien, Kenneth R.; Yoshimura, Akihiko.
：: Nature Immunology, 巻 4, 番号 6, 01.06.2003, p. 551-556.研究成果: Article
}
TY - JOUR
T1 - IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages
AU - Yasukawa, Hideo
AU - Ohishi, Masanobu
AU - Mori, Hiroyuki
AU - Murakami, Masaaki
AU - Chinen, Takatoshi
AU - Aki, Daisuke
AU - Hanada, Toshikatsu
AU - Takeda, Kiyoshi
AU - Akira, Shizuo
AU - Hoshijima, Masahiko
AU - Hirano, Toshio
AU - Chien, Kenneth R.
AU - Yoshimura, Akihiko
PY - 2003/6/1
Y1 - 2003/6/1
N2 - Whereas interleukin-6 (IL-6) is a proinflammatory cytokine, IL-10 is an anti-inflammatory cytokine. Although signal transducer and activator of transcription 3 (STAT3) is essential for the function of both IL-6 and IL-10, it is unclear how these two cytokines have such opposing functions. Here we show that suppressor of cytokine signaling 3 (SOCS3) is a key regulator of the divergent action of these two cytokines. In macrophages lacking the Socs3 gene or carrying a mutation of the SOCS3-binding site in gp130, the lipopolysaccharide-induced production of tumor necrosis factor (TNF) and IL-12 is suppressed by both IL-10 and IL-6. SOCS3 specifically prevents activation of STAT3 by IL-6 but not IL-10. Taken together, these data indicate that SOCS3 selectively blocks signaling by IL-6, thereby preventing its ability to inhibit LPS signaling.
AB - Whereas interleukin-6 (IL-6) is a proinflammatory cytokine, IL-10 is an anti-inflammatory cytokine. Although signal transducer and activator of transcription 3 (STAT3) is essential for the function of both IL-6 and IL-10, it is unclear how these two cytokines have such opposing functions. Here we show that suppressor of cytokine signaling 3 (SOCS3) is a key regulator of the divergent action of these two cytokines. In macrophages lacking the Socs3 gene or carrying a mutation of the SOCS3-binding site in gp130, the lipopolysaccharide-induced production of tumor necrosis factor (TNF) and IL-12 is suppressed by both IL-10 and IL-6. SOCS3 specifically prevents activation of STAT3 by IL-6 but not IL-10. Taken together, these data indicate that SOCS3 selectively blocks signaling by IL-6, thereby preventing its ability to inhibit LPS signaling.
UR - http://www.scopus.com/inward/record.url?scp=0037600741&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0037600741&partnerID=8YFLogxK
U2 - 10.1038/ni938
DO - 10.1038/ni938
M3 - Article
C2 - 12754507
AN - SCOPUS:0037600741
VL - 4
SP - 551
EP - 556
JO - Nature Immunology
JF - Nature Immunology
SN - 1529-2908
IS - 6
ER -