Academic literature on the topic 'ST2/IL-33'
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Journal articles on the topic "ST2/IL-33"
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Dwyer, Gaelen K., Lisa R. Mathews, Anna Lucas, Bruce R. Blazar, and Heth R. Turnquist. "Recipient conditioning contributes to IL-33-driven Th1 alloimmune responses following rapid ST2 upregulation on donor CD4+ T cells during lymphopenia-induced proliferation." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 55.4. http://dx.doi.org/10.4049/jimmunol.200.supp.55.4.
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Abstract IL-33 is augmented in recipient tissues by conditioning before allogeneic stem cell transplantation (alloSCT) and is a required signal to donor T cell for GVHD. Targetable mechanisms by which IL-33 supports GVHD are yet undefined. Conditioning causes lymphopenia-induced proliferation (LIP) and releases microbial products. These products promote myeloid cell secretion of IL-12, which induces the IL-33 receptor, ST2, on T cells in vitro. We hypothesized that IL-12 induces ST2 on donor T cells during LIP promoting IL-33 augmentation of the Th1 responses leading to GVHD. To establish the role of IL-12 in T cell ST2 expression and IL-33-mediated GVHD, irradiated BALB/c mice were given B6 alloSCT and T cells. Some mice received IL-12p40 neutralizing Ab or control Ab alone, with or without concurrent IL-33 administration. To test the impact of lymphopenia on T cells, ST2−Foxp3−CD4+ T cells alone or with ST2+ Treg were transferred into B6 Rag2−/−γc−/− mice. Mice received PBS or IL-33 on days 1–8. Neutralizing IL-12 did not reduce ST2 on T cells after alloSCT nor rescue mice from IL-33-mediated acceleration of GVHD. Post-alloSCT, IL-33 worked with IL-12 to expand ST2+Tbet+ Th1 cells. Neutralizing IL-12, but not delivery of IL-33, increased Gata3+ Th2 cells after alloSCT. During LIP, CD4+Foxp3− T cells rapidly upregulated ST2 independent of IL-33, but IL-33 then favored the expansion of Th1 cells, even in the presence of ST2+ Treg. These data suggest that CD4+ T cells rapidly upregulate ST2 during alloSCT conditioning induced lymphopenia. After alloSCT, IL-33 does not support Treg or Th2 cells, but works with IL-12 to augment Th1 responses and GVHD. Blocking stimuli that induces ST2 on proliferating donor CD4+ T cells may be effective for limiting GVHD.
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Matta, Benjamin, Jeremy Lott, Lisa Mathews, Brian Rosborough, and Heth Turnquist. "CD11c+ dendritic cells are required for IL-33-mediated expansion of ST2+Foxp3+ regulatory T cells in vivo (P1075)." Journal of Immunology 190, no. 1_Supplement (May 1, 2013): 121.9. http://dx.doi.org/10.4049/jimmunol.190.supp.121.9.
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Abstract IL-33 is an IL-1 cytokine that signals via ST2, which is expressed on T cells and myeloid cells. Although IL-33 promotes Th2 responses, its administration potently expands CD4+Foxp3+ regulatory T cells (Treg). We examined if IL-33 expands murine Treg directly or indirectly through its impact on CD11c+ DC. The ability of IL-33 to facilitate CD3/CD28-stimulated proliferation of wild-type (WT) or ST2-/- Treg was compared to IL-2. The impact of IL-33 on the capacity of DC to expand Treg was defined in vitro on bone marrow (BM)-generated DC from WT or ST2-/- mice and in vivo using CD11c-DTR BM chimeras administered diphtheria toxin (DT) to deplete CD11c+ cells during IL-33 treatment. The capacity of IL-33-expanded Treg from Foxp3-RFP reporter mice to suppress effector T cells was assessed. We found that IL-33 directly expands Treg in vitro, including an ST2+ subset absent from IL-2-treated cultures. IL-33-exposed DC generate ST2+ Treg from naïve T cells, and is dependent on ST2 expressed by DC. IL-33 failed to expand Treg in vivo, especially ST2+ Treg, in the absence of CD11c+ cells. In conclusion, IL-33 promotes the expansion of suppressive Foxp3+ Treg, including an ST2+ subset in vitro and in vivo. This results from IL-33 activity directly on Treg, but more significantly, indirectly through its impact on CD11c+ cells. These findings have important implications for further characterization of ST2+ Treg and the development of novel therapeutics aimed at promoting immune tolerance.
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Zhao, Qing, and Guangjie Chen. "Role of IL-33 and Its Receptor in T Cell-Mediated Autoimmune Diseases." BioMed Research International 2014 (2014): 1–10. http://dx.doi.org/10.1155/2014/587376.
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Interleukin-33 (IL-33) is a new cytokine of interleukin-1 family, whose specific receptor is ST2. IL-33 exerts its functions via its target cells and plays different roles in diseases. ST2 deletion and exclusion of IL-33/ST2 axis are accompanied by enhanced susceptibility to dominantly T cell-mediated organ-specific autoimmune diseases. It has been reported that IL-33/ST2 pathway plays a key role in host defense and immune regulation in inflammatory and infectious diseases. This review focuses on new findings in the roles of IL-33 and ST2 in several kinds of T cell-mediated autoimmune diseases.
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Matta, Benjamin, Jeremy Lott, Lisa Mathews, Brian Rosborough, Bruce Blazar, and Heth Turnquist. "IL-33 stimulates dendritic cell secretion of IL-2 that promotes selective expansion of ST2+Foxp3+ regulatory T cells (IRC5P.460)." Journal of Immunology 192, no. 1_Supplement (May 1, 2014): 125.9. http://dx.doi.org/10.4049/jimmunol.192.supp.125.9.
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Abstract IL-33 is a pleiotropic IL-1 family cytokine that signals via ST2 and expands ST2+Foxp3+ regulatory T cells (Treg) in vivo. As ST2+ Treg show poor expansion by direct IL-33 stimulation, we sought to define mechanisms mediating their expansion. IL-2 signaling promotes ST2 expression on CD4+ T cells, and dendritic cells (DC) express ST2 (able to respond to IL-33), and are a potential source of IL-2. Thus, we examined if IL-33 mediates ST2+ Treg expansion by stimulating DC IL-2 production. CD11c+ wild type (WT) or IL-2 knockout (KO) bone marrow DC were exposed to IL-33 or LPS. DC phenotype was evaluated by multi-color flow cytometric analysis. The influence of IL-33 DC on T cell function was evaluated in MLR with CD4+ T cells, and T cell proliferation and phenotype were determined by flow analysis. Cytokines were quantitated by ELISA. We found that unlike LPS, IL-33 does not influence DC surface phenotype or induce pro-inflammatory cytokine production compared to controls. However, IL-33 induces a 5-fold increase IL-2 production by DC. In MLR, IL-33 DC selectively expand an activated subset of ST2+Foxp3+ Treg that are CD44hiICOShi. IL-33 DC-derived IL-2 is critical since IL-33-exposed IL-2 KO DC fail to expand ST2+ Treg. In summary, IL-33 licenses DC to selectively expand a subset of activated Treg through production of IL-2, in the absence of classical DC activation. These findings may be harnessed to aid the development of novel therapeutics aimed at promoting immune tolerance.
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Song, Yitian, Fangzhi Wei, Ying Liu, Feng Han, Lihui Ma, Yanping Zhuang, Chengdan Pan, Zhandong Jia, and Aimin Gong. "IL-33/ST2 Activation Is involved in Ro60-Regulated Photosensitivity in Cutaneous Lupus Erythematosus." Mediators of Inflammation 2022 (July 20, 2022): 1–15. http://dx.doi.org/10.1155/2022/4955761.
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Interleukin- (IL-) 33 contributes to various inflammatory processes. IL-33/ST2 activation participates in systemic lupus erythematous via binding to the receptor of Suppression of Tumorigenicity 2 protein (ST2). However, whether IL-33/ST2 interferes with the nosogenesis of cutaneous lupus erythematosus (CLE) has not been reported so far. Herein, we proposed to disclose the impacts on IL-33/ST2 activation and Ro60 on CLE and their potential implications in the photosensitization of CLE cells. IL-33, ST2, and Ro60 in CLE patients’ skin lesions were detected. Murine keratinocytes stimulated with or without IL-33 were irradiated by ultraviolet B (UVB), and the levels of Ro60 and inflammation markers were determined. Keratinocytes were cocultured with J774.2 macrophages and stimulated with IL-33 for analysis of chemostasis. The results identified that IL-33, ST2, and downstream inflammation markers were significantly upregulated in CLE lesions with Ro60 overexpression. Additionally, IL-33 treatment promoted the upregulation of Ro60 induced by UVB treatment in murine keratinocytes. Moreover, IL-33 stimulates keratinocytes to induce macrophage migration via enhancing the generation of the chemokine (C–C motif) ligands 17 and 22. Meanwhile, the silencing of ST2 or nuclear factor-kappa B (NF-κB) suppression abolished IL-33-induced upregulation of Ro60 in keratinocytes. Similarly, the inhibition of SOX17 expression was followed by downregulation of Ro60 in keratinocytes following IL-33 stimulation. In addition, UVB irradiation upregulated SOX17 in keratinocytes. Conclusively, the IL-33/ST2 axis interferes with Ro60-regulated photosensitization via activating the NF-κB- and PI3K/Akt- and SOX17-related pathways.
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Zhang, Xiaoli, Benjamin M. Matta, Dawn K. Reichenbach, Bruce R. Blazar, and Heth R. Turnquist. "Suppression of Tumorigenicity 2 (ST2) signaling is required for regulatory T cell control of Graft-vs. Host Disease." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 140.20. http://dx.doi.org/10.4049/jimmunol.196.supp.140.20.
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Abstract How IL-33-mediated signals impact on ST2-expressing regulatory T cell (Treg) expansion and regulatory functions is poorly understood. To establish the importance of direct IL-33 stimulation of Treg for control of alloimmune responses, we utilized a rodent model of graft-vs. host disease (GVHD) where C57BL/6 mice were irradiated and given a BALB/c bone marrow transplant (BMT) along with BALB/c CD4+ CD25+ Treg from st2+/+ or st2−/− mice at a 1:2 ratio with WT BALB/c CD3+ effector T cells. As expected, WT st2+/+ CD4+ CD25+ cells promoted full protection against GVHD with 90% of recipients receiving st2+/+ CD4+ CD25+ free of GVHD at Day 100 post-BMT. However, only 10% of mice that received st2−/− Treg achieved long-term survival (p=0.0017, st2+/+ v. st2−/−). Associated mechanistic studies revealed that Treg frequency was significantly reduced in recipients receiving st2−/− Treg compared to those receiving st2+/+ Treg. To define the signaling patterns IL-33 generates in Treg, fluorescence activated cell sorting was used to obtain ST2− or ST2+ Treg cells from the splenocytes of Foxp3 reporter mice and IL33 activated signaling downstream of ST2 was quantitated by phosphoflow cytometry. This analysis revealed that IL-33 signaling via ST2 on Treg activates both NF-κB and p38 MAPK. Yet, only IL-33-stimulated p38 MAPK, but not NF-kB, signaling was required for ST2+ Treg expansion. Our studies make two important observations regarding how IL-33 stimulation of Treg supports immune regulation. First, we demonstrate that IL-33 activates p38 MAPK to drive selective ST2+ Treg expansion. Second, we show that IL-33-mediated signals are critical to the capacity of Treg to control the alloimmune responses leading to GVHD.
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Han, Jae Ho, Chang-Hee Suh, Ju-Yang Jung, Mi-Hyun Ahn, Ji Eun Kwon, Hyunee Yim, and Hyoun-Ah Kim. "Serum Levels of Interleukin 33 and Soluble ST2 Are Associated with the Extent of Disease Activity and Cutaneous Manifestations in Patients with Active Adult-onset Still’s Disease." Journal of Rheumatology 44, no. 6 (April 1, 2017): 740–47. http://dx.doi.org/10.3899/jrheum.170020.
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Objective.Interleukin 33 (IL-33), a member of the IL-1 family and a ligand of the orphan receptor ST2, plays key roles in innate and adaptive immunity. We examined the associations between IL-33/ST2 levels and clinical manifestations of patients with active adult-onset Still’s disease (AOSD).Methods.Blood samples were collected from 40 patients with active AOSD, 28 patients with rheumatoid arthritis (RA), and 27 healthy controls (HC). The serum levels of IL-33 and soluble ST2 were determined using ELISA. Expression levels of IL-33 and ST2 in biopsy specimens obtained from 34 AOSD patients with rash were immunohistochemically investigated.Results.IL-33 levels of patients with AOSD were higher than those of patients with RA and HC. Soluble ST2 levels of patients with AOSD were higher than those of HC, but not of patients with RA. Serum IL-33 levels correlated with systemic score, erythrocyte sedimentation rate, ferritin levels, and aspartate transaminase levels. However, serum soluble ST2 levels correlated only with ferritin levels. The numbers of inflammatory cells expressing IL-33 and ST2 were elevated in skin lesions of patients with AOSD compared to HC, but did not differ from those of the skin lesions of eczema or psoriasis.Conclusion.We found significantly higher serum IL-33 and soluble ST2 levels in patients with active AOSD. Results indicate that the IL-33/ST2 signaling pathway may play a role in the pathogenesis of the acute inflammation and skin manifestations associated with AOSD.
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Dong, Yonghua, Hua Hu, Dandan Fu, Shuting Zheng, Qingqing Wang, Keshav K C, Xiangfeng Song, and Zhongwei Tian. "Serum Expression of IL-33 and ST2 in Patients with Psoriasis Vulgaris." Archives of Iranian Medicine 24, no. 9 (September 1, 2021): 689–95. http://dx.doi.org/10.34172/aim.2021.99.
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Background: Psoriasis vulgaris (PsV) is an immune-mediated skin disease of unknown mechanism. Interleukin 33 (IL-33) is a member of IL-1 cytokine family and suppression of tumorigenicity 2 (ST2) is the specific ligand of IL-33. It has been found that IL-33 and ST2 are increased in psoriatic lesions, but the expression levels in serum and their relationship to clinical features are still unclear. The aim of this study is to assess IL-33, ST2, IL-17 and IL-5 serum levels as well as serum concentration of blood glucose and blood lipids in PsV patients and their relationship with clinical characteristics. Methods: Sixty-eight PsV samples and 60 healthy individuals were recruited. Serum levels of IL-33, ST2, IL-17 and IL-5 were measured by enzyme-linked immunosorbent assay and blood glucose and blood lipid were assayed by automatic biochemical analyzer. Results: Serum levels of IL-33, ST2, IL-17 and IL-5 were increased significantly in PsV patients compared with controls (P<0.01). Cytokines were overexpressed in PsV patients during active stages compared with controls (P<0.05). Expression levels of IL-33, ST2 and IL-17 confirmed a significance in different severity groups of PsV patients (P<0.05). Serum concentration of triglyceride (TG) was also increased compared with controls (P=0.024). IL-33 levels were positively correlated with total cholesterol (TC) levels (r=0.319, P=0.008). Conclusion: IL-33/ST2 could generally reflect the activity and disease severity in PsV patients, which indicates that the IL-33/ST2 signaling pathway plays an important role in the pathogenesis of PsV.
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Johnston, Laura K., Chia-Lin Hsu, Rebecca A. Krier-Burris, Krishan D. Chhiba, Karen B. Chien, Andrew McKenzie, Sergejs Berdnikovs, and Paul J. Bryce. "Eosinophil lineage commitment and IL-5-dependent expansion is regulated by IL-33 in mice." Journal of Immunology 196, no. 1_Supplement (May 1, 2016): 191.7. http://dx.doi.org/10.4049/jimmunol.196.supp.191.7.
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Abstract Eosinophils are important in the pathogenesis of many diseases, including asthma, eosinophilic esophagitis and eczema. While IL-5 is necessary for the maturation of eosinophil progenitors (EoP) into mature eosinophils (EoM), the signals that promote commitment to the eosinophil lineage are unknown. The IL-33 receptor, ST2, is expressed on several inflammatory cells, including eosinophils, and is best characterized for its role during the initiation of allergic responses in the peripheral tissues. Recently, ST2 expression was described on hematopoietic stem cells, where its function remains unclear. Here, we sought to determine whether IL-33 and ST2 contribute to hematopoietic lineage decisions. We found that both IL-33- and ST2-deficient mice exhibited diminished peripheral blood eosinophils at baseline. Correspondingly, IL-33 administration increased EoM as well as IL-5 in the blood and bone marrow in WT and IL-33-deficient but not ST2-deficient mice. Blocking IL-5 with a neutralizing antibody prevented IL-33-expanded EoP from maturing into EoM, while transgenic overexpression of IL-5 in ST2-deficient mice resulted in significantly lower hypereosinophilia than transgenic IL-5 mice. Finally, we observed that IL-33, but not IL-5, specifically expanded EoP and upregulated IL-5Rα on EoP as well as increased IL-5 after bone marrow was cultured for three days. Our findings identify a basal defect in eosinophilopoiesis in IL-33- and ST2-deficient mice. Furthermore, we establish unappreciated roles for IL-33 and ST2 in eosinophil development via progenitor regulation and define a mechanism whereby IL-33 licenses commitment into the eosinophil lineage by driving both responsiveness to IL-5 and IL-5 production.
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Li, Yun-Qiu, Yu Zhong, Xu-Ping Xiao, Dan-Dan Li, Zheng Zhou, and Yan-Yan Tian. "IL-33/ST2 axis promotes the inflammatory response of nasal mucosal epithelial cells through inducing the ERK1/2 pathway." Innate Immunity 26, no. 6 (May 26, 2020): 505–13. http://dx.doi.org/10.1177/1753425920918911.
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Allergic rhinitis (AR) is a nasal mucosal inflammatory disease mediated by environmental allergens. At present, the relationship between the IL-33/ST2 axis, ERK1/2 pathway and AR progression needs further exploration. In our study, an AR model was constructed in vitro by treating HNEpC cells with Der p1. qRT-PCR was applied to assess the mRNA levels of IL-33, ST2, TNF-α, IL-6, and IL-8. Western blotting was used to measure the protein levels of IL-33, ST2, and the downstream proteins p-ERK1/2, ERK1/2, p-RSK, and RSK. IL-6, IL-8, IL-33, and TNF-α protein levels in cell supernatants were evaluated by ELISA. Flow cytometry was performed to check cell apoptosis of HNEpC in the presence or absence of Der p1. Our results indicate that the relative levels of IL-33, ST2, TNF-α, IL-6, and IL-8 were increased significantly in the AR model group. The above effects were notably reversed after transfection with shIL-33 or shST2. IL-33 stimulation further resulted in the increase in both ST2 and inflammation-associated cytokines, and these effects were restored after shST2 treatment. Also, the levels of inflammatory factors induced by IL-33 stimulation or ST2 overexpression were reversed after applying an ERK1/2 pathway blocker. In conclusion, IL-33/ST2 mediated inflammation of nasal mucosal epithelial cells by inducing the ERK1/2 pathway.
Dissertations / Theses on the topic "ST2/IL-33"
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Arshad, Muhammad Imran. "Role of IL-33/ST2 axis in acute hepatitis." Rennes 1, 2012. http://www.theses.fr/2012REN1B103.
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L'interleukine-33 (IL-33), une cytokine de type alarmine de la famille de l’IL-1, est essentiellement exprimée par les cellules endothéliales et les cellules épithéliales dans diverses pathologies inflammatoires chez la souris et chez l'Homme. IL-33 induit son activité biologique par l'interaction d’un récepteur hétérodimérique composé de ST2 et IL-1RAcP. Les nouvelles sources cellulaires de l'IL-33 et la régulation de son expression restent mal connues dans le foie. L'objectif de ma thèse était de mieux comprendre les mécanismes d'expression, de régulation et d’activité de l'IL-33 en tant qu’alarmine au cours des hépatites aiguës murines induites par CCl4, ConA, FasL/Jo2, D-GalN-TNFα, Poly(I:C) et MHV3 ainsi que chez les patients souffrant d’hépatite fulminante à VHB. Nous avons montré que l’IL-33 était surexprimée dans tous les modèles hépatiques étudiés chez la souris avec une expression dans les cellules endothéliales sinusoïdales du foie et les cellules endothéliales vasculaires. L'IL-33 dont l'expression est associée à l'hypervascularisation du foie a également été observée chez les patients atteints d’hépatites fulminantes à VHB. Plus surprenant, nous avons trouvé que l'IL-33 était inductible dans les hépatocytes au cours des hépatites à ConA, à Poly(I:C) et induites par le MHV3 chez la souris. Nous avons démontré que les cellules NKT et la cytokine de mort cellulaire TRAIL, régulaient l’expression de l’IL-33 dans les hépatocytes au cours de l’hépatite à ConA. De plus, la nécroptose (ou nécrose programmée) dépendante des kinases PARP-1, RIPK1 et RIPK3 contrôle l’expression de l’IL-33 dans les hépatocytes au cours de l’hépatite à ConA. Ceci aboutit au concept d’IL-33 comme marqueur de la nécroptose. Au niveau fonctionnel, l’IL-33 a un effet protecteur dans les dommages hépatiques induits par la ConA suggérant un rôle bénéfique de l’axe IL-33/ST2 dans certaines pathologies du foie. En conclusion, nous mettons en évidence que les cellules NKT, la molécule TRAIL, la molécule PARP-1 et les kinases RIPK1, -3 contrôlent l’expression de l'IL-33 dans la physiopathologie de foie. Ces résultats suggèrent un rôle important de l’axe IL-33/ST2 dans les maladies du foieInterleukin-33 (IL-33), an alarmin cytokine of IL-1 family, is primarily expressed by endothelial cells and epithelial cells in various inflammatory pathologies in mice and human. IL-33 mediates its biological activity by interaction with specific ST2 and IL-1RAcP receptors. The novel cellular sources of IL-33 and its regulation particularly in liver remain obscure. The objective of my thesis was to better determine the expression, regulation and functions of IL-33 as an alarmin during murine acute hepatitis induced by CCl4, ConA, FasL/Jo2, D-GalN-TNF-α, Poly(I:C) and MHV3 as well as in human patients suffering from HBV fulminant hepatitis. IL-33 was over-expressed in all studied murine hepatic models with induced expression in liver sinusoidal endothelial cells and vascular endothelial cells. The IL-33 over-expression associated with hypervascularisation was also found in HBV fulminant hepatic patients. More surprisingly, we found that IL-33 was expressed in hepatocytes during ConA, Poly(I:C) and MHV3 mediated acute hepatitis in mice. We demonstrated that NKT cells and cell death inducing molecule TRAIL regulated the hepatocyte-specific IL-33 expression during ConA-hepatitis. The PARP-1-RIPK1-RIPK3 mediated necroptosis (or programmed necrosis) in ConA liver injury regulated IL-33 expression in hepatocytes. This leads to the concept of IL-33 as a marker of necroptosis. At functional level, IL-33 had a protective impact in ConA-induced liver injury supporting the current protective role of IL-33/ST2 axis in liver pathology. In conclusion, we evidence a novel NKT cells, TRAIL, PARP-1 and RIP kinases dependent regulatory mechanism for IL-33 in liver pathophysiology. These findings suggest an important role of IL-33/ST2 axis in liver diseases
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Alyahyaei, Zahraa. "The role of IL-33 and ST2 in early pregnancy." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:a6fd7c02-feeb-4fe5-b8e1-5713a65653b9.
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Regulation of the growth and differentiation of trophoblast cells is critical for successful embryo implantation and placentation. Cytokines are key players in these processes, as well as modulating the maternal immune response to prevent rejection of the conceptus. This thesis focused on the investigation of the cytokine interleukin (IL) - 33 and its receptor, ST2. ST2 has two isoforms, a functional cell surface receptor (ST2L) and a soluble decoy receptor (sST2). Previous work in this laboratory had shown that the human placenta expresses both IL-33 and sST2 at term. The aim of this thesis was to investigate IL-33 and ST2 in early pregnancy, the time when trophoblast is at its most active, with a view to better understanding their role. IL-33 and ST2 mRNA and protein were examined in 14 first trimester placentas from 6-12 weeks of gestation. IL-33 was localized to cells in the villous stroma, whereas ST2 was present in the syncytiotrophoblast, villous cytotrophoblast and the invasive extravillous cytotrophoblast of the cell columns. Secretion of sST2, but not IL-33, by the placenta was found. Investigation of pre-implantation embryos showed the presence of ST2, but not IL-33 protein. Decidualized endometrium was investigated as a potential source of IL-33 and sST2 at the maternal-fetal interface and, although mRNA for both was present, no protein could be found. The key finding was that sST2, rather than ST2L, was the predominant isoform in the placenta. This led us to reconsider the hypothesis that IL-33/ST2 interactions in the placenta are important for successful pregnancy and raised the possibility that they may have independent roles. Using trophoblast cell lines as a model, it was shown that sST2 binds to trophoblast cells, significantly inhibits their proliferation and stimulates their invasion in vitro. This is the first report of this novel role for sST2 in pregnancy. Thus these studies have shown that sST2 may play an important role in implantation and placentation through controlling trophoblast invasion.
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Murphy, Grace E. J. "IL-33 and ST2 in innate and adaptive airway inflammation." Thesis, University of Glasgow, 2015. http://theses.gla.ac.uk/6685/.
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Background: ST2 has been identified in playing an important role in Th2-mediated inflammation and asthma. IL-33 acts as the ligand for ST2; it is a novel cytokine that induces innate Th2/type-2 responses when delivered to the lung. The hierarchy of IL-33 and type-2 cytokines and chemokines in Th2 inflammation in the lung has not been fully elucidated. Furthermore, the role of IL-33 in the adaptive response in allergic mediated airways disease is unclear. Epithelial cells (ECs) are increasingly recognised as having an immunological role in airway inflammation and asthma, in particular releasing cytokines such as IL-33. Little is known about whether ST2 is expressed on these cells and what function IL-33 responsive ECs may have in Th2 diseases. Soluble ST2 (sST2) has emerged as a biomarker correlating with disease activity in cardiovascular disease. It is not known if there is a clear association between sST2 and asthma, nor whether measurable IL-33 concentrations are present and if so, their association with disease severity. The influence of smoking and corticosteroid treatment on these parameters has also not been determined. Aim: To ascertain the levels of systemic sST2 and IL-33 in asthmatic patients. To determine cytokine, chemokine and airway dynamics of IL-33-driven innate airway inflammation. To determine the role of epithelial cells in IL-33-driven innate airway inflammation. To investigate the function of ST2/IL-33 axis in the innate and adaptive responses in allergic airways inflammation and asthma. Methods and Results: sST2 and IL-33 levels in plasma of never smokers, ex-smokers and smokers were determined by immunoassay before and after a corticosteroid trial. Corticosteroid treatment resulted in increased sST2 levels in all smoking status patient groups; there was no effect attributable to smoking. Time course and dosage interval experiments were performed in mice treated with intranasal IL-33. IL-5, IL-13, eotaxin/CCL11 and eotaxin2/CCL24 mediated eosinophilic airway inflammation (AI). Treatment of mice with both anti- CCL11 and -CCL24 partially ameliorated the AI. IL-4 gene deficient mice were protected from IL-33-induced inflammation. BALB/c mice displayed airways hyperreactivity following IL-33 treatment. Murine, human cell line and primary human ECs were assessed for ST2 expression by immunohistochemistry and fluorescence activated cell sorting (FACS). ST2 expression was clearly demonstrated in the ECs. Subsequently ECs were treated with IL-33 in an in vitro setting including in a pseudostratifed epithelium model. ECs produced a range of inflammatory and angiogenic mediators in response to IL-33. In particular IL-33 driven EC-derived VEGF promoted angiogenesis in vitro. Intranasal IL-33 induced increased endothelial cells and vascular remodelling in vivo. Experimental allergic airways inflammation (AAI) was generated in BALB/c mice which were co-treated with IL-33 or PBS at allergen sensitisation. IL-33 induced the polarisation of IL-5+IL-4- T cells in the draining lymph nodes and these mice developed more severe inflammation. AAI was induced in WT, ST2-deficient, IL-4-deficient and ST2/IL-4 deficient mice. These experiments showed IL-4 was necessary for generation of AAI which could not be overcome by ST2-pathway stimulation in an adjuvant-free model. Conclusions: The data presented further extends the current understanding of the ST2/IL-33 axis in the innate and adaptive aspects of Th2 inflammation in AAI and asthma. In particular the hierarchy of mediators and cells involved in Th2 inflammation, including at the sensitisation phase, have been explored. This identifies ST2/IL-33 as a potential target in the development of biological therapies for asthma.
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Pitman, Nicholas Ian. "The role of IL-33 and ST2 in allergic airways disease." Thesis, University of Glasgow, 2010. http://theses.gla.ac.uk/1817/.
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Asthma is a chronic disease characterised by variable airflow obstruction, bronchial hyperresponsiveness and airways inflammation. At an immunological level Th2 inflammation and the presence of activated eosinophils and mast cells are key features of asthma. ST2, the receptor for the novel cytokine IL-33, is expressed upon Th2 lymphocytes and mast cells but its role in clinical and experimental asthma remains unclear. IL-33 has been shown to induce local and systemic eosinophilia when administered to the peritoneum of mice. In this thesis I have set out to test the hypothesis that the activation of mast cells by IL-33 acting on cell surface ST2 plays a critical role in allergic airways inflammation. I began by studying the function of ST2 on mast cells in vitro. I found that ST2 was expressed at an early stage of development, and correlated closely with the expression of the stem cell factor receptor (c-kit), a marker present on mast cells from a progenitor stage. Despite this mast cells generated form ST2 gene deleted mice proliferated and matured normally. When mast cells were activated by IL-33, acting in an ST2-dependent manner, pro-inflammatory cytokines and chemokines were released that have potential roles in asthma, specifically IL-6, IL-13, MIP-1α and MCP-1. To extend these findings I looked at the role of ST2 in allergic airways inflammation. I first optimised and validated an ovalbumin and adjuvant based ‘short’ twelve day model of murine asthma and demonstrated that ST2 gene deletion results in attenuated eosinophilic inflammation. In addition to being ST2 dependent it is possible that this adjuvant based short model is mast cell dependent, unlike longer adjuvant based models which are mast cell and ST2 independent. Therefore I went on to study an adjuvant-free model of asthma which has been demonstrated to be mast cell dependent. In this adjuvant-free model of asthma the airway inflammation was attenuated in ST2 gene deficient mice compared with wild type mice, while AHR was unaffected. There was an associated reduction in IgE production and thoracic lymph node recall Th2 cytokine responses. I then examined the effect of ST2 activation in the lungs. When IL-33 was administered directly to the airways of naïve mice it induced the features of experimental asthma. There was extensive eosinophilic inflammation within the lung tissue and airspaces. The Th2 cytokines IL-5 and IL-13, and the eosinophil chemoattractant chemokines eotaxin-1 and eotaxin-2 were detected at increased concentrations. Significant airways hyperresponsiveness was also generated. Using ST2 gene deleted mice I demonstrated that these effects were ST2 specific. Although I have shown that mast cells are activated by IL-33 in vitro, I used mast cell deficient mice to demonstrate that the eosinophilic inflammation generated by IL-33 is unaffected by the absence of mast cells. These data show that IL-33 can induce in the lungs the cardinal pathological characteristics of asthma, and that it appears to act upstream of other important mediators such as IL-13 and the eotaxins. Furthermore the IL-33 receptor ST2 is required in an adjuvant free model of asthma, which is more akin to human disease. Placing these findings in the context of recent evidence that IL-33 is released by structural cells in response to damage or injury suggests that IL-33 may play a key role in initiating the immunological features of clinical asthma. As a consequence of this position in the hierarchy of inflammation IL-33 offers a promising direct target for novel biological therapies in asthma.
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Kewin, Peter. "The role of IL-33 and ST2 in innate and adaptive inflammation." Thesis, University of Glasgow, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.444379.
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Ferrari, Larissa Staurengo. "Participação da IL-33/ST2 em modelo de artrite séptica em camundongos." Universidade Estadual de Londrina. Centro de Ciências Biológicas. Programa de Pós-Graduação em Patologia Experimental, 2011. http://www.bibliotecadigital.uel.br/document/?code=vtls000163964.
Full textAbstract:
A preparação da suspensão bacteriana e o intervalo de confiança de UFC nessa suspensão é um importante procedimento utilizado em laboratórios como métodos para avaliação de respostas inflamatórias e pode ser obtido por diferentes métodos, tais como diuições seriadas e pela análisa visual da turbidez através da escala de McFarland. Nós investigamos a influência do armazenamento da suspensão de Staphylococcus aureus na viabilidade de bactérias e sua influência na inflamação induzida por essa suspensão. O armazenamento da suspensão de S. aureus a 8 º C por 24 h diminuiu a viabilidade bacteriana não só em suspensões preparadas por diluições seriadas, mas também ao seguirmos a escala de McFarland 0,5. O aumento do tempo de armazenamento reduziu o número de UFC de S. aureus. Como conseqüência da viabilidade bacteriana reduzida, foi detectada redução do recrutamento de leucócitos em um modelo de peritonite bacteriana. Em modelo de artrite séptica foi detectada redução da hiperalgesia mecânica, edema e recrutamento de leucócitos. Esses resultados demonstram que o armazenamento da suspensão bacteriana afeta a viabilidade bacteriana e também a resposta inflamatória "in vivo". Uma solução possível para determinar/estimar o número de UFC é o uso da escala de McFarland, que permitirá a elaboração e utilização de uma suspensão bacteriana no mesmo dia para testes in vivo e assim, evita-se a diminuição da viabilidade bacteriana e a influência de resultados experimentais.The preparation of bacterial suspension is an important procedure used in laboratories for inflammatory evaluation protocols and can be obtained by different methods such as CFU (colony forming unities), needs storage counting and McFarland scale turbidity (does not need storage). We investigated the influence of storage of Staphylococcus aureus suspension as bacterial viability and its influence in bacteria-induced inflammation. . The increase of time of storage reduced the S. aureus CFU. As a consequence of reduced bacterial viability, it was detected reduced leukocyte recruitment in a model of bacterial peritonitis, and reduced mechanical hyperalgesia, edema and leukocyte recruitment in septic arthritis. These results demonstrate that storage of bacterial suspension affected bacterial viability and also the inflammatory response in vivo, raising the importance of standard procedures for bacterial suspension preparation. A conceivable approach would be to determine the number of CFU at a specific McFarland"s scale degree, which will allow the preparation and use a bacterial suspension in the same day for in vivo testing and avoiding reduced bacterial viability.
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Li, Xiaofei. "The IL-33/ST2 pathway in CNS : Traumatic brain injury and brain tumour." Thesis, Uppsala universitet, Institutionen för biologisk grundutbildning, 2012. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-183937.
Full textAbstract:
Interleukin 33 (IL-33) is a dual function cytokine. It is a member of the IL-1 family and it acts as a pro-inflammatory factor (18 kilo Dalton, 18 kD) like other cytokines in IL-1 family. IL-33 is also a transcription factor (32 kD - form) which can suppress or activate gene transcription in diverse cases. A variety of cell types and tissues in the central nervous system (CNS) can release IL-33 after injury. The 18 kD IL-33 binds to the membrane receptor protein ST2 ligand, then regulates downstream gene expression, triggers cytokine synthesis, and modulates the immune system response. After traumatic brain injury (TBI) in the CNS, glial cells become key players in the nervous tissue response. Astrocytes undergo activation, proliferation, release pro-inflammatory factors and, as a consequence, a glial scar barrier around the injury is formed. Simultaneously, resting microglia are activated and able to remove debris. Lastly, oligodendrocytes together with microglia and astrocytes are activated and communicate with the immune system. In addition, as a severe kind of injury to the CNS, brain tumours share some similar characteristics of brain injury, such as hypoxia and inflammation. Therefore, IL-33 may play a role in neuroinflammation and also in brain tumours. In this project, our aim was to investigate the role of IL-33 and the IL-33/ST2 pathway in traumatic brain injury and brain tumours (e.g glioma). We found that IL-33 can influence the CNS immune resonse, and may be important in CNS pathology.
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Amôr, Nádia Ghinelli. "Papel do receptor ST2 no desenvolvimento de carcinoma espinocelular induzido quimicamente." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/25/25149/tde-26042016-112036/.
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O carcinoma espinocelular (CEC) é um dos cânceres humanos mais incidentes. A despeito do entendimento da fisiopatologia do CEC, as opções terapêuticas ainda são limitadas e o(s) exato(s) mecanismo(s) envolvido(s) na progressão deste tipo de tumor ainda não foi descrito. Estudos recentes mostram a existência de uma associação direta entre a resposta imune TH1 e um melhor prognóstico em pacientes com CEC. Aumento da expressão de componentes do eixo IL-33/ST2 foi demonstrado contribuir para transformação neoplásica em diversos modelos tumorais, incluindo cânceres de estômago e de mama. Trabalho recente do nosso e de outros laboratórios indicam que IL-33 pode impedir a resposta imune TH1 . Baseado nessas observações, a hipótese testada foi que o impedimento da resposta imune pela interação IL-33/ST2 pode contribuir para iniciação e progressão do CEC. Utilizando modelo de carcinogênese química em camundongos WT e deficientes de ST2 (ST2KO), os resultados mostram que a deficiência de ST2 leva a uma notável redução da severidade das lesões 20 semanas após a carcinogênese química, sugerindo que a sinalização ST2 é necessária para o desenvolvimento tumoral neste modelo. Análises do infiltrado inflamatório presente nas lesões em camundongos WT e ST2KO revelaram redução significativa nas percentagens de macrófagos, células T CD4+ e células dendríticas, mas não em células T CD8+, células B e células natural killer (NK) no microambiente tumoral de camundongos ST2KO. Além disso, células NK esplênicas isoladas de camundongos ST2KO exibiram atividade citotóxica aumentada contra células YAC quando comparado com células de camundongos do grupo controle (WT). Os resultados indicam que a via IL-33/ST2 contribui para o desenvolvimento de carcinoma espinocelular recrutando células T CD4+, macrófagos e células dendríticas e reduzindo a citotoxicidade de células NK.Squamous cell carcinoma (SCC) is the second most common form of skin cancer and is most commonly observed in photo-exposed areas of the body. The mechanism(s) involved in the progression of this tumor are unknown. Recent studies have shown that there is a direct association between a TH1-related immune response and a better prognosis in patients with SCC. Increased expression of the IL33/ST2 axis components has been demonstrated to contribute to neoplastic transformation in several tumor models, including gastric and breast cancer. Recent work from ours and other laboratories indicate that can IL-33 impair TH1-type immune responses. Based on these observations, we hypothesized that TH1-type immune response impairment by IL33/ST2 could contribute to the initiation and progress SCC. We found that ST2 deficiency led to a marked decreased in severity of skin lesions at 20 weeks post-DMBA, suggesting that ST2 signaling is necessary for tumor development in this model. Analysis of tumor lesions in WT and ST2KO mice revealed that lack of ST2 led to a specific and significant reduction in the frequency of macrophages, T CD4+ and dendritic cells, but not CD8+, B and NK cells. In addition, splenic NK cells isolated from DMBA-treated ST2KO mice exhibited increased cytotoxicity activity against YAC cells targets when compared with WT splenic NK cells in the same cytotoxic assay. Altogether, our findings indicate that IL-33/ST2 pathway contributes to the SCC development by recruitment T CD4+ cells, macrophages, and dendritic cells and impairing NK cytotoxicity.
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Stolarski, Bartosz. "The role of IL 33/ST2 pathway in innate immune response in airway inflammation." Thesis, University of Glasgow, 2011. http://theses.gla.ac.uk/2961/.
Full textAbstract:
Asthma is a common and complex inflammatory disease of the airways characterized by deregulated immune responses that involves activation of multiple cell types including Th2 cells, IgE producing B cells, mast cells, basophils and eosinophils as well as resident lung cells such as epithelial, smooth muscle cells and macrophages. Despite intensive research, there are still unmet needs in the treatment of asthma. Recently, a new cytokine of IL 1 family, named IL 33 emerged as a potentially important factor in the immunopathogenesis of allergy and asthma. It was recently shown in our laboratory that intranasal administration of IL 33 can induce certain physiological features that are characteristic of experimental asthma, such as eosinophilic inflammation, Th2 cytokine and antibody production as well as increased airway hyperresponsiveness. The effect of IL 33 on the activation and differentiation of allergen specific Th2 cells has been well studied. However, the contribution of IL 33 to the activation of lung resident and inflammatory innate cells remains undefined. In this project I focused on alveolar macrophages and eosinophils as both cell types were reported to express IL 33R, ST2L and are thought to play a crucial role in asthma pathogenesis. I raised the hypothesis that IL 33 released locally in the lungs may trigger symptoms resembling asthma through the activation of airway alveolar macrophages. Furthermore, I hypothesize that IL 33 may exacerbate and maintain inflammation in the lungs by the direct activation of eosinophils. In our previous study we showed that IL 33 could switch the quiescent phenotype of alveolar macrophages toward the alternatively activated phenotype (M2, AAM). In the first part of my thesis I looked at the consequences of this phenomenon for airway inflammation. Using clodronate liposomes in vivo I was able to eliminate macrophage population from the lungs and demonstrated that resident alveolar macrophages are crucial for the development of IL 33 induced eosinophilic inflammation in the airways. I then examined the contribution of IL 13, a known M2 differentiation factor, to airway inflammation. Using anti IL 13 neutralizing antibodies I showed that IL 13 is required for the IL 33 triggered differentiation of alveolar macrophages toward M2 phenotype as well as for eosinophilic inflammation. Next, I looked at how IL 33/ST2 pathway modulates the differentiation and activation of eosinophil. I demonstrated that bone marrow hematopoietic progenitors CD117+ express ST2L and that IL 33 is able to differentiate these cells toward eosinophils. By employing deficient mice or neutralizing antibodies I found that this process is ST2 and IL 5 dependent and independent of IL 13. I then extended my research interests to include mature mouse and human eosinophils. I showed that both human and mouse resting eosinophils express low levels of ST2L which can be markedly increased by IL 33. Moreover, I demonstrated that eosinophils that are recruited to the lungs during experimental allergic airway inflammation express high levels of ST2L. Furthermore, I carried out a study on effector function of eosinophils. I found that IL 33 induces IL 13, IL 6 and increases TARC, TGF production by mouse eosinophils. In addition, IL 33 exacerbated IgG induced human and mouse eosinophil degranulation, likely by enhancing FcRII expression. Having shown earlier that IL 13 is requited for the polarization of alveolar macrophages toward AAM by IL 33 in vitro and in light of the fact that IL 33 stimulated eosinophils can be a significant source of IL 13; I went on to investigate the interaction between macrophages and eosinophils. Using co cultures of ST2 / macrophages with WT eosinophils in Transwell system, I demonstrated that IL 33 but not IL 5 activated eosinophils can support macrophage polarization toward the pro inflammatory AAM phenotype, partially through the production of IL 13. Finally, given the role of IL 33/ST2L axis in eosinophil activation in vitro, I investigated the contribution of IL 33 activated eosinophils to airway inflammation in vivo. Using adoptive transfer protocol I showed that the contribution of IL 33 activated eosinophils to airway inflammation is mediated primarily by the release of cytokines from these cells which, in turn, recruits other inflammatory cells and supports the differentiation of alveolar macrophages towards AAM. These data show that IL 33/ST2 pathway regulates multiple features of alveolar macrophage and eosinophil biology that can have a significant impact on asthma pathophysiology in the airways. Studies carried out in our laboratory and elsewhere suggest that IL 33 is equally capable of activating other cell types that have been implicated in asthma pathology such as Th2, B1 cells, DCs, mast cells and basophils. Therefore, targeting IL 33/ST2 pathway may potentially offer a promising therapeutic approach to asthma and allergy.
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Bignardi, Letícia Andreotti. "Estudo do papel do eixo IL-33/ST2 na progressão da lesão periapical experimental." Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/58/58135/tde-02022015-114411/.
Full textAbstract:
A citocina IL-33 apresenta papel dual e está envolvida com a resolução ou progressão de inúmeras doenças, além disso, acredita-se que a via IL-33/ST2 esteja envolvida no equilíbrio entre a atividade de osteoclastos e osteoblastos. O objetivo deste estudo foi avaliar o papel do receptor ST2 no desenvolvimento e progressão de lesões periapicais experimentalmente induzidas em camundongos. Lesões periapicais foram induzidas em primeiros molares inferiores de camundongos WT e ST2 knockout (KO). Decorridos 7 e 14 dias, as amostras de mandíbula foram submetidas às análises: determinação da área de lesão periapical em cortes histológicos e do volume por microtomografia computadorizada (μCT); contagem de osteoclastos submetidos ao ensaio de histoenzimologia (TRAP); expressão gênica de marcadores osteogênicos e osteoclastogênicos por q-PCR; quantificação de neutrófilos por ensaio de mieloperoxidases. Os linfonodos foram submetidos à análise da expressão dos fatores transcricionais T-bet, GATA-3, RORc e Foxp-3 por q-PCR. Análise estatística utilizada foi One-way ANOVA, seguido de pós-teste de Bonferroni. Aos 14 dias, observou-se maior extensão da lesão periapical em animais WT que em ST2KO (p<0,05). O tamanho da lesão nos animais ST2KO permaneceu igual em função do tempo. Foi observada maior quantidade de neutrófilos na lesão do grupo WT aos 7 dias, em comparação aos animais ST2KO (p<0,05). Na expressão de T-bet, GATA-3, RORc e Foxp-3 não foram observadas diferenças estatisticamente significantes. O número de osteoclastos contados nos animais ST2KO foi maior que o observado em WT aos 7dias e aos 14 dias (p<0,05). A expressão de Runx2 foi maior no grupo lesão dos animais ST2KO quando comparado a seu respectivo controle. Os outros marcadores relacionados com a formação óssea não apresentaram diferenças estatisticamente significantes. Dentre os marcadores relacionados com a reabsorção óssea, a catepsina K e o MMP-9 apresentaram maior expressão aos 14 dias, na lesão dos animais WT quando comparada à expressão na lesão dos animais ST2KO (p<0,05). Com base nos resultados obtidos no presente estudo, pode-se concluir que na ausência do receptor ST2 as lesões periapicais são menos extensas e embora em maior quantidade, os osteoclastos são menos ativos. Nossos resultados sugerem um importante papel da via IL-33/ST2 na ativação dos osteoclastos e desenvolvimento da lesão periapical.The IL -33 cytokine presents a dual role and is involved either in the resolution and progression of many diseases. Furthermore, it is believed that this pathway is involved between osteoclast and osteoblast activity balance. The aim of this study was to evaluate the role of ST2 receptor in the development and progression of experimentally induced periapical lesions in mice. Periapical lesions were induced in first molars of WT and ST2 knockout (KO) mice. After 7 and 14 days, jaw samples were subjected to various analysis: determination of periapical lesions area by histology and volume by computed microtomography (μCT); osteoclasts number by TRAP histoenzymology; osteogenic and osteoclastogenic markers expression by q-PCR; neutrophil quantification by myeloperoxidase activity. The expression of transcription factors T-bet, GATA-3, RORC and Foxp-3 in lymph nodes were analysed by q-PCR. Statistical analysis was done by One-way ANOVA and Bonferroni post-test. It was observed a greater extent in periapical lesions of WT compared to ST2KO animals at 14 days (p<0.05). There is no progression in the lesion of ST2KO mice with the time. A larger number of neutrophils in WT group was observed, compared to ST2KO mice evaluated at 7 days (p<0.05). The expression of T-bet, GATA-3, RORc and Foxp-3 were not statistically significant different among the groups. The number of osteoclasts in lesions of ST2KO animals were greater than the observed in WT, at 7 and 14 days (p<0.05). Although, other osteogenic markers showed no statistically significant difference, Runx2 expression in ST2KO was higher in lesion side compared to control side at 14 days. The markers related to bone resorption, cathepsin K and MMP-9, were significantly abrogated in the lesion side of ST2KO mice, at 14 days (p<0.05). Based on the results, it can be concluded that although larger amounts of osteoclast were counted in ST2KO, the lesion was less extensive and osteoclasts less active. It all suggests that the IL-33/ST2 pathway play an important role in osteoclasts activation and periapical lesion development.
Book chapters on the topic "ST2/IL-33"
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Borges, Amanda, Melissa Abreu, Camila Miguel, Javier Emilio Lazo-Chica, and Wellington Rodrigues. "EIXO IL-33/ST2 NA DOENÇA PERIODONTAL CRÔNICA NA SENESCÊNCIA: UM ESTUDO ANALÍTICO TRANSVERSAL." In Perspectivas em Saúde: Saberes epidemiológicos, Ciência e Comunidade, 44–52. Editora Creative, 2021. http://dx.doi.org/10.53924/pswr.04.
Full textConference papers on the topic "ST2/IL-33"
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Church, Colin, Ammad Mahmood, Charles McSharry, Damo Xu, Andrew Peacock, and David J. Welsh. "An ST2/IL-33 Transgenic Mouse Model Of Pulmonary Hypertension." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4975.
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Li, J., J. M. Magat, J. L. Thomas, and J. P. Dumouchel. "Endogenous IL-33 and Its Auto-Amplification of IL-33/ST2 Pathway Play an Important Role in Asthma." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2945.
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Wang, Yang, and Bin Wang. "Research Progress of IL-33/ST2 Signaling Pathway in Cardiovascular Disease." In Proceedings of the 2018 8th International Conference on Management, Education and Information (MEICI 2018). Paris, France: Atlantis Press, 2018. http://dx.doi.org/10.2991/meici-18.2018.98.
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Cohen, Suzanne, Ian Scott, Jayesh Majithiya, Laura Rapley, Benjamin Kemp, Nicholas Bond, Dorothy Sims, et al. "LATE-BREAKING ABSTRACT: Oxidation of the alarmin IL-33 regulates ST2-dependent inflammation." In Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa292.
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Gordon, Erin D., Margaret Solon, Prescott Woodruff, and John V. Fahy. "Dysregulation Of IL-33 And ST2 In Stable Asthma And Acute Asthma Exacerbations." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4269.
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Yu, S. L., Y. B. Huo, C. H. Huang, Y. Tao, W. H. Huang, C. K. Wong, L. S. Tam, et al. "SAT0043 Il-33/st2-mediated inflammation in endothelial cell is directly aggravated by il-6 during lupus nephritis." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6064.
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Scott, I. C., E. England, D. G. Rees, T. Erngren, C. Chaillan Huntington, K. F. Houslay, D. A. Sims, et al. "Tozorakimab: a dual-pharmacology anti-IL-33 antibody that inhibits IL-33 signalling via ST2 and RAGE/EGFR to reduce inflammation and epithelial dysfunction." In ERS International Congress 2022 abstracts. European Respiratory Society, 2022. http://dx.doi.org/10.1183/13993003.congress-2022.2467.
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Yu, S., and Y. Tao. "AB0056 Emerging role of IL-33/ST2 axis in endothelial cell injury of lupus nephritis." In Annual European Congress of Rheumatology, 14–17 June, 2017. BMJ Publishing Group Ltd and European League Against Rheumatism, 2017. http://dx.doi.org/10.1136/annrheumdis-2017-eular.1700.
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Dustin, C., C. Schiffers, D. E. Heppner, M. Hristova, A. Habibovic, and A. Van Der Vliet. "DUOX1-Dependent IL-33 Secretion from the Airway Epithelium Involves Positive Feedback Signaling Through Activation of IL-33R/ST2." In American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a2829.
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Neumann, K., F. Heinrich, A. Ochel, and G. Tiegs. "The alarmin IL-33 drives a ST2+ Treg-mediated anti-inflammatory immune response during immune-mediated hepatitis." In 35. Jahrestagung der Deutschen Arbeitsgemeinschaft zum Studium der Leber. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0038-1677273.
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