Soluble ST2 suppresses IL-5 production by human basophilic KU812 cells, induced by epithelial cell-derived IL-33

Matsumoto, Koji; Kouzaki, Hideaki; Kikuoka, Hirotaka; Kato, Tomohisa; Tojima, Ichiro; Shimizu, Shino; Shimizu, Takeshi

doi:10.1016/j.alit.2018.05.009

Cited by 7 publications

(8 citation statements)

References 37 publications

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“…The enhanced sST2 presence has been shown to inhibit the production of the type 2 cytokines IL-4 and IL-5 but not the type 1 cytokine interferon-γ. (45) sST2 could act as a moderator of inflammation, but more evidence is needed to confirm the extent of the ability of sST2 to moderate inflammation in AIH.…”

Section: Discussionmentioning

confidence: 99%

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Abe¹,

Takahashi²,

Fujita³

et al. 2019

Hepatol Commun

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Interleukin (IL)‐33 was recently described as a new member of the IL‐1 family; members of this family have proinflammatory activity. IL‐33 and its soluble receptor ST2 (sST2) have been implicated in the pathogenesis of autoimmune diseases. This study investigated serum IL‐33 and sST2 in type I autoimmune hepatitis (AIH) and the relationship of these molecules with clinical and pathologic parameters. Subjects included 65 patients with AIH who were diagnosed in our hospital. The control population included 17 healthy individuals and 36 patients with primary biliary cholangitis (PBC). Mean age at AIH diagnosis was 55.5 years, and the male‐to‐female ratio was 6:59. Serum IL‐33 and sST2 levels were significantly higher in patients with AIH than in those with PBC or controls. Importantly, immunohistochemistry revealed high IL‐33 expression in liver sections from patients with AIH. In particular, serum IL‐33 and sST2 levels were significantly higher in acute‐onset AIH than in chronic‐onset AIH. Serum IL‐33 levels were positively correlated with serum total bilirubin (TB), alanine aminotransferase (ALT), and necroinflammatory activity in AIH. We performed multivariate logistic regression analysis and found serum IL‐33 levels to be independent factors for severe activity. Serum sST2 levels were positively correlated with serum TB and ALT and negatively correlated with serum albumin and prothrombin time in AIH. In particular, serum sST2 levels were significantly higher in severe symptoms of AIH. Serum IL‐33 and sST2 levels in patients with AIH responsive to treatment with prednisolone were significantly decreased after treatment. Interestingly, serum IL‐33 level was associated with a significantly increased risk of relapse. Conclusion: IL‐33/ST2 may play an important role in the pathogenesis and severity of AIH and may be a promising target for AIH therapy.

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Section: Discussionmentioning

confidence: 99%

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Abe¹,

Takahashi²,

Fujita³

et al. 2019

Hepatol Commun

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“…DAMP-related molecules have been confirmed to be expressed abnormally in ACLF patients, and IL-33, sST2 ( 28 , 30 , 32 , 106 ), and HMGB1 ( 58 ) have also been found to be single biomarkers that predict the prognosis of ACLF. There is currently no ACLF therapy targeting DAMPs, but neutralization of IL-33 ( 130 ) using sST2, HMGB1, and IL-33-blocking antibodies ( 131 – 133 ) and TSA-acetylated histones ( 53 ) can effectively reduce the inflammatory cytokine storm caused by DAMPs, which shows the potential of ACLF precision immune diagnosis and treatment targeting DAMPs.…”

Section: Summary and Perspectivesmentioning

confidence: 99%

The Immune Pathogenesis of Acute-On-Chronic Liver Failure and the Danger Hypothesis

Qiang

Liu

2022

Front. Immunol.

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Acute-on-chronic liver failure (ACLF) is a group of clinical syndromes related to severe acute liver function impairment and multiple-organ failure caused by various acute triggering factors on the basis of chronic liver disease. Due to its severe condition, rapid progression, and high mortality, it has received increasing attention. Recent studies have shown that the pathogenesis of ACLF mainly includes direct injury and immune injury. In immune injury, cytotoxic T lymphocytes (CTLs), dendritic cells (DCs), and CD4+ T cells accumulate in the liver tissue, secrete a variety of proinflammatory cytokines and chemokines, and recruit more immune cells to the liver, resulting in immune damage to the liver tissue, massive hepatocyte necrosis, and liver failure, but the key molecules and signaling pathways remain unclear. The “danger hypothesis” holds that in addition to the need for antigens, damage-associated molecular patterns (DAMPs) also play a very important role in the occurrence of the immune response, and this hypothesis is related to the pathogenesis of ACLF. Here, the research status and development trend of ACLF, as well as the mechanism of action and research progress on various DAMPs in ACLF, are summarized to identify biomarkers that can predict the occurrence and development of diseases or the prognosis of patients at an early stage.

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“…The p50 is essential for the expression of transcription factor GATA-3 that can regulate the Th2 cytokine genes expression. 6,27,28 On the other hand, the sST2 level is elevated in asthma and also plays a critical role in Th2 cell-mediated diseases. In fact, sST2 effectively attenuated inflammatory responses and Th2 cytokines production and negatively regulates the Th2 cell-mediated immunological responses.…”

Section: The Il-33 Genementioning

confidence: 99%

“…Also, the p50 and c‐Rel have a role in the development of allergic airway inflammation. The p50 is essential for the expression of transcription factor GATA‐3 that can regulate the Th2 cytokine genes expression 6,27,28 …”

Section: The Il‐33 Genementioning

confidence: 99%

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IL‐33/ST2 pathway as upper‐hand of inflammation in allergic asthma contributes as predictive biomarker in heart failure

et al. 2022

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Allergic asthma is an inflammatory disorder of the bronchi, and as a major health problem, more than 350 million people suffer from asthma in the world. Many cardiovascular disorders resulted in the impairment of the heart's power to pump blood that leads to the HF. More than 25 million people worldwide live with HF. Accordingly, identifying the biomarkers to predict the onset of future asthma and HF is necessary. IL‐33 is an inflammatory cytokine that has the main role in pathophysiology of asthma and HF. Also, in IL‐33 receptor, the ST2 is involved in cardiac fibrosis and remodelling in HF and pathogenesis of allergic asthma. Increased sST2 in allergic asthma helps to control inflammation during asthma, but increased sST2 in HF is a predictable biomarker to present risk factor of HF during the time of the patients.

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Soluble ST2 suppresses IL-5 production by human basophilic KU812 cells, induced by epithelial cell-derived IL-33

Abstract: Epithelial cell-derived IL-33 promoted IL-5 production by KU812 cells. The subsequently produced sST2 has important roles in regulating Th2 responses.

Cited by 7 publications

References 37 publications

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

Interleukin‐33/ST2‐Mediated Inflammation Plays a Critical Role in the Pathogenesis and Severity of Type I Autoimmune Hepatitis

The Immune Pathogenesis of Acute-On-Chronic Liver Failure and the Danger Hypothesis

IL‐33/ST2 pathway as upper‐hand of inflammation in allergic asthma contributes as predictive biomarker in heart failure

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