IL-6 induces an anti-inflammatory response in the absence of SOCS3 in macrophages
By H. Yasukawa, M. Ohishi, H. Mori, M. Murakami, T. Chinen, Daisuke Aki, Toshikatsu Hanada, K. Takeda, Shizuo Akira, M. Hoshijima and 3 more. Nature Immunology, 2003
841 citations recorded by the source corpus.
Subfields: Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/3307195afb91cb5a83ebf1eafb1d854eb8a37823
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Citations in the corpus
- Regulation of JAK–STAT signalling in the immune system (2003, background): “Conditional Socs3 gene-targeting studies have shown an important role for SOCS3 in the negative regulation of interleukin-6 (IL-6) signalling in macrophage”
- Immunomodulatory functions of type I interferons (2012, background): “Interestingly, other receptors, such as the IL-6 receptor, can activate STAT3, but this does not result in an anti-inflammatory response, possibly owing to the participation of additional regulatory factors, such as members of the suppressor of cytokine signalling (SOCS) famil”
- SOCS proteins, cytokine signalling and immune regulation (2007, background): “SOCS3 has now been shown to be a key regulator for the divergent activity of IL-6 and IL-10 following TLR stimulatio”
- The STAT3 isoforms α and β have unique and specific functions (2004, background): “The suppressor of cytokine signaling 3 gene ( Socs3 ) is a good candidate for this, because it is involved in negative regulation of IL-6 signalin”
- The JAK-STAT Signaling Pathway: Input and Output Integration1 (2007, neutral): “By contrast, receptors that are regulated by SOCS3 cannot activate the anti-inflammatory response, such as the IL-6R (37, 67).”
- Suppressors of cytokine signaling and immunity (2003, background): “In macrophages lacking Socs3 or carrying a mutation in the SOCS3-binding site (Y759F) of gp130, not only IL-10, but also IL-6, suppresses LPS-induced TNF productio”