Th17 cells and their associated cytokines in liver diseases

Lafdil, Fouad; Miller, Andrew M.; Ki, Sung Hwan; Gao, Bin

doi:10.1038/cmi.2010.5

Cited by 131 publications

(114 citation statements)

References 58 publications

Supporting

Mentioning

106

Contrasting

Order By: Relevance

“…Otherwise, H. pylori DNA was not detected in the liver of patients with alcoholic cirrhosis and those with autoimmune hepatitis. In agreement with previous studies (Straubinger et al 2003, Algood & Cover 2006, Lafdil et al 2010, we confirmed the strong Th1 proinflammatory response with increased levels of IFN-γ, the Th1 signature cytokine, in these patients. We F: female; M: male; n: number of subjects; SD: standard deviation.…”

Section: Discussionsupporting

confidence: 80%

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

Silva

Rocha

et al. 2011

Mem. Inst. Oswaldo Cruz

View full text Add to dashboard Cite

The hypothesis that Helicobactermight be a risk factor for human liver diseases has arisen after the detection of Helicobacter DNA in hepatic tissue of patients with hepatobiliary diseases. Nevertheless, no explanation that justifies the presence of the bacterium in the human liver has been proposed. We evaluated the presence of Helicobacterin the liver of patients with hepatic diseases of different aetiologies. We prospectively evaluated 147 patients (106 with primary hepatic diseases and 41 with hepatic metastatic tumours) and 20 liver donors as controls. Helicobacter species were investigated in the liver by culture and specific 16S rDNA nested-polymerase chain reaction followed by sequencing. Serum and hepatic levels of representative cytokines of T regulatory cell, T helper (Th)1 and Th17 cell lineages were determined using enzyme linked immunosorbent assay. The data were evaluated using logistic models. Detection of Helicobacter pylori DNA in the liver was independently associated with hepatitis B virus/hepatitis C virus, pancreatic carcinoma and a cytokine pattern characterised by high interleukin (IL)-10, low/absent interferon-γ and decreased IL-17A concentrations (p < 10-3). The bacterial DNA was never detected in the liver of patients with alcoholic cirrhosis and autoimmune hepatitis that are associated with Th1/Th17 polarisation. H. pylori may be observed in the liver of patients with certain hepatic and pancreatic diseases, but this might depend on the patient cytokine profile

show abstract

Section: Discussionsupporting

confidence: 80%

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

Silva

Rocha

et al. 2011

Mem. Inst. Oswaldo Cruz

View full text Add to dashboard Cite

show abstract

“…IL-17F, originally named for and derived from Th-17-producing T cells, is primarily a proinflammatory cytokine that is involved in innate immunity and autoimmune diseases (reviewed in reference 41). The IL-17 receptor is widely expressed in immune cells, fibroblasts, and epithelial cells, including Huh-7 liver cells (42,43). Our results show that IL-17F induced ISRE-mediated ISG expression, particularly in combination with IFN; these effects required Stat1 signaling and involved endogenous IFN-␤.…”

Section: Discussionmentioning

confidence: 61%

Human Cytokinome Analysis for Interferon Response

Al-Yahya

Mahmoud

Al-Zoghaibi

et al. 2015

J Virol

View full text Add to dashboard Cite

IMPORTANCE Innate immunity to viruses is an early defense system to ward off viruses. One mediator is interferon (IFN), which activates a cascade of biochemical events that aim to control the virus life cycle. In our work, we examined more than 200 cytokines, soluble mediators produced within the body as a result of infection, for the ability to enhance IFN action. We identified enhanced interactions with specific IFNs and cytokines. We also revealed that betacellulin, IL-17, and IL-11 cytokines have the novel property of enhancing the antiviral action of IFN against several viruses. These results demonstrate that the human genome codes for previously unknown proteins with unrelated functions that can augment the innate immunity to viruses. Knowing these interactions not only helps our understanding of immunity to viruses and emerging diseases, but can also lead to devising possible new therapeutics by enhancing the mediator of antiviral action itself, IFN.

show abstract

“…IL-17A plays a critical role in neutrophil recruitment, angiogenesis, inflammation, and autoimmune disease that has been previously described extensively (6), including in pulmonary and cardiac fibrosis via IL-17RA and MAPK signaling (8,9). However, very few studies have investigated the role of IL-17A in liver fibrosis (10).…”

mentioning

confidence: 99%

IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation

Tan

Qian

Jiang

et al. 2013

The Journal of Immunology

269

208

View full text Add to dashboard Cite

Liver fibrosis is a severe, life-threatening clinical condition resulting from nonresolving hepatitis of different origins. IL-17A is critical in inflammation, but its relation to liver fibrosis remains elusive. We find increased IL-17A expression in fibrotic livers from HBV-infected patients undergoing partial hepatectomy because of cirrhosis-related early-stage hepatocellular carcinoma in comparison with control nonfibrotic livers from uninfected patients with hepatic hemangioma. In fibrotic livers, IL-17A immunoreactivity localizes to the inflammatory infiltrate. In experimental carbon tetrachloride–induced liver fibrosis of IL-17RA–deficient mice, we observe reduced neutrophil influx, proinflammatory cytokines, hepatocellular necrosis, inflammation, and fibrosis as compared with control C57BL/6 mice. IL-17A is produced by neutrophils and T lymphocytes expressing the Th17 lineage–specific transcription factor Retinoic acid receptor–related orphan receptor γt. Furthermore, hepatic stellate cells (HSCs) isolated from naive C57BL/6 mice respond to IL-17A with increased IL-6, α-smooth muscle actin, collagen, and TGF-β mRNA expression, suggesting an IL-17A–driven fibrotic process. Pharmacologic ERK1/2 or p38 inhibition significantly attenuated IL-17A–induced HSC activation and collagen expression. In conclusion, IL-17A+ Retinoic acid receptor–related orphan receptor γt+ neutrophils and T cells are recruited into the injured liver driving a chronic, fibrotic hepatitis. IL-17A–dependent HSC activation may be critical for liver fibrosis. Thus, blockade of IL-17A could potentially benefit patients with chronic hepatitis and liver fibrosis.

show abstract

Th17 cells and their associated cytokines in liver diseases

Cited by 131 publications

References 58 publications

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

The presence of Helicobacter pylori in the liver depends on the Th1, Th17 and Treg cytokine profile of the patient

Human Cytokinome Analysis for Interferon Response

IL-17A Plays a Critical Role in the Pathogenesis of Liver Fibrosis through Hepatic Stellate Cell Activation

Contact Info

Product

Resources

About