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. 2002 Nov;17(5):583-91.
doi: 10.1016/s1074-7613(02)00446-6.

SOCS1/JAB is a negative regulator of LPS-induced macrophage activation

Ichiko Kinjyo  1 , Toshikatsu Hanada, Kyoko Inagaki-Ohara, Hiroyuki Mori, Daisuke Aki, Masanobu Ohishi, Hiroki Yoshida, Masato Kubo, Akihiko Yoshimura
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Free article

SOCS1/JAB is a negative regulator of LPS-induced macrophage activation

Ichiko Kinjyo et al. Immunity. 2002 Nov.
Free article

Abstract

Bacterial lipopolysaccharide (LPS) triggers innate immune responses through Toll-like receptor (TLR) 4. We show here that the suppressor of cytokine-signaling-1 (SOCS1/JAB) is rapidly induced by LPS and negatively regulates LPS signaling. SOCS1(+/-) mice or SOCS1(-/-) mice with interferon-gamma (IFNgamma)-deficient background were more sensitive to LPS-induced lethal effects than were wild-type littermates. LPS-induced NO(2)(-) synthesis and TNFalpha production were augmented in SOCS1(-/-) macrophages. Furthermore, LPS tolerance, a protection mechanism against endotoxin shock, was also strikingly reduced in SOCS1(-/-) cells. LPS-induced I-kappaB and p38 phosphorylation was upregulated in SOCS1(-/-) macrophages, and forced expression of SOCS1 suppressed LPS-induced NF-kappaB activation. Thus, SOCS1 directly suppresses TLR4 signaling and modulates innate immunity.

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