Interleukin 22 (IL-22) plays a protective role in T cell-mediated murine hepatitis: IL-22 is a survival factor for hepatocytes via STAT3 activation

Radaeva, Svetlana; Sun, Rui; Pan, Hongna; Hong, Feng; Gao, Bin

doi:10.1002/hep.20184

Cited by 536 publications

(568 citation statements)

References 44 publications

(57 reference statements)

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“…Using different methods to manipulate cytokine signaling, they were able to show that STAT3 activity is essential for the protection of the liver against inflammation. Intriguingly, IL-22 seems to play a major protective role in the Con A hepatitis model (58). Both of these examples stress the concept that STAT3 activity, be it regulated by IL-10 or other cytokines in other tissues, is essential for anti-inflammatory pathways.…”

Section: Generation Of the Air In Diverse Pathological Scenariosmentioning

confidence: 95%

General Nature of the STAT3-Activated Anti-Inflammatory Response

Kasmi

Holst²,

Coffre

et al. 2006

The Journal of Immunology

201

179

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Although many cytokine receptors generate their signals via the STAT3 pathway, the IL-10R appears unique in promoting a potent anti-inflammatory response (AIR) via STAT3 to antagonize proinflammatory signals that activate the innate immune response. We found that heterologous cytokine receptor systems that activate STAT3 but are naturally refractory (the IL-22R), or engineered to be refractory (the IL-6, leptin, and erythropoietin receptors), to suppressor of cytokine signaling-3-mediated inhibition activate an AIR indistinguishable from IL-10. We conclude that the AIR is a generic cytokine signaling pathway dependent on STAT3 but not unique to the IL-10R.

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Section: Generation Of the Air In Diverse Pathological Scenariosmentioning

confidence: 95%

General Nature of the STAT3-Activated Anti-Inflammatory Response

Kasmi

Holst²,

Coffre

et al. 2006

The Journal of Immunology

201

179

View full text Add to dashboard Cite

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“…Another cytokine, IL-22 induced phosphorylation of STAT3 on a serine residue and has been shown to induce acute phase genes in the liver [67], an effect that has been described to be regulated by IL-6 mainly through STAT3 activation. It has been shown that STAT3 Ser727 phosphorylation is induced upon IL-22 stimulation and is required for maximal transcriptional activation [68].…”

Section: Inflammationmentioning

confidence: 99%

Potential role of signal transducer and activator of transcription (STAT)3 signaling pathway in inflammation, survival, proliferation and invasion of hepatocellular carcinoma

Subramaniam

Shanmugam

Perumal

et al. 2013

Biochimica et Biophysica Acta (BBA) - Reviews on Cancer

202

229

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a b s t r a c t a r t i c l e i n f oHepatocellular carcinoma (HCC) is one of the most lethal malignancies, and is also the fourth most common cancer worldwide with around 700,000 new cases each year. Currently, first line chemotherapeutic drugs used for HCC include fluorouracil, cisplatin, doxorubicin, paclitaxel and mitomycin, but most of these are non-selective cytotoxic molecules with significant side effects. Sorafenib is the only approved targeted therapy by the U.S. Food and Drug Administration for HCC treatment, but patients suffer from various kinds of adverse effects, including hypertension. The signal-transducer-and-activator-of-transcription 3 (STAT3) protein, one of the members of STATs transcription factor family, has been implicated in signal transduction by different cytokines, growth factors and oncogenes. In normal cells, STAT3 activation is tightly controlled to prevent dysregulated gene transcription, whereas constitutively activated STAT3 plays an important role in tumorigenesis through the upregulation of genes involved in anti-apoptosis, proliferation and angiogenesis. Thus, pharmacologically safe and effective agents that can block STAT3 activation have the potential both for the prevention and treatment of HCC. In the present review, we discuss the possible role of STAT3 signaling cascade and its interacting partners in the initiation of HCC and also analyze the role of various STAT3 regulated genes in HCC progression, inflammation, survival, invasion and angiogenesis.

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“…IL-22 has recently been shown to be preferentially expressed by the Th17 subset [41,42] and has been demonstrated as a strong activator of STAT3 [43][44][45] . Recently, we have demonstrated that IL-22 contributes to rapid amelioration of local inflammation associated with a Th2-mediated colitis through activation of STAT3 in CECs [46] (Figure 1).…”

Section: The Role Of Stat3-activators On Ibdmentioning

confidence: 99%

Role of STAT3 in inflammatory bowel disease

Sugimoto¹

2008

WJG

111

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Signal transducers and activators of transcription 3 (STAT3) play an important role in various autoimmune disorders including inflammatory bowel disease (IBD). Recent studies have revealed that STAT3 activation plays distinctly different roles between innate immune responses and acquired immune responses in colitis. STAT3-mediated activation of acquired immune responses plays a pathogenic role in colitis by enhancing the survival of pathogenic T cells. In contrast, STAT3-mediated activation of innate responses contributes to the suppression of colitis. This review will summarize the current understanding of the roles of STAT3 in IBD and the potential of targeting STAT3 for the treatment of IBD, emphasizing recent observations.

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Interleukin 22 (IL-22) plays a protective role in T cell-mediated murine hepatitis: IL-22 is a survival factor for hepatocytes via STAT3 activation

Cited by 536 publications

References 44 publications

General Nature of the STAT3-Activated Anti-Inflammatory Response

General Nature of the STAT3-Activated Anti-Inflammatory Response

Potential role of signal transducer and activator of transcription (STAT)3 signaling pathway in inflammation, survival, proliferation and invasion of hepatocellular carcinoma

Role of STAT3 in inflammatory bowel disease

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