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Articles de revues sur le sujet « ST2/IL-33 »

Auteur : Grafiati

Publié le 9 mars 2023

Mis à jour le 31 juillet 2025

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1

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 (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

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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 (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-DT

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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 (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 phenotyp

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Song, Yitian, Fangzhi Wei, Ying Liu, et al. "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

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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 (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 recipient

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Han, Jae Ho, Chang-Hee Suh, Ju-Yang Jung, et al. "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 (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

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Dong, Yonghua, Hua Hu, Dandan Fu, et al. "Serum Expression of IL-33 and ST2 in Patients with Psoriasis Vulgaris." Archives of Iranian Medicine 24, no. 9 (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 characte

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Johnston, Laura K., Chia-Lin Hsu, Rebecca A. Krier-Burris, et al. "Eosinophil lineage commitment and IL-5-dependent expansion is regulated by IL-33 in mice." Journal of Immunology 196, no. 1_Supplement (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 re

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Cao, Shujun, Xuyong Qin, Chengping Li, et al. "The IL-33/ST2 Axis Affects Adipogenesis Through Regulating the TRAF6/RelA Pathway." International Journal of Molecular Sciences 25, no. 22 (2024): 12005. http://dx.doi.org/10.3390/ijms252212005.

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Understanding the regulatory mechanisms of adipogenesis is essential for preventing obesity. Interleukin-33 (IL-33) has recently attracted increasing attention for its role in adipogenesis. The purpose of this study was to explore the function and regulatory mechanism of IL-33 and its receptor suppression of tumorigenicity 2 (ST2) on adipogenesis. Here, Oil Red O staining was used to detect the accumulation of intracellular lipid droplets. Molecular techniques such as qRT-PCR and Western blotting were used to detect the expression of pivotal genes and adipogenic marker genes. Gains and losses

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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 (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 evaluat

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Begum, Salma, Barry E. Perlman, Nuriban Valero-Pacheco, et al. "Dynamic Expression of Interleukin-33 and ST2 in the Mouse Reproductive Tract Is Influenced by Superovulation." Journal of Histochemistry & Cytochemistry 68, no. 4 (2020): 253–67. http://dx.doi.org/10.1369/0022155420911049.

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Interleukin-33 (IL-33) is an IL-1 family cytokine with pleiotropic effects on diverse cell types. Dysregulated IL-33 signaling has been implicated in pregnancy-related disorders, including preeclampsia and recurrent pregnancy loss, and in ovarian function in women undergoing controlled ovarian stimulation for in vitro fertilization. To date, expression of IL-33 and its receptor subunit, ST2, in the female reproductive tract remains poorly characterized. We identify IL-33-expressing oocytes surrounded by ST2-expressing granulosa cells at all stages of follicular development, in addition to IL-3

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Chen, Wei-Yu, Tzu-Hsien Tsai, Jenq-Lin Yang, and Lung-Chih Li. "Therapeutic Strategies for Targeting IL-33/ST2 Signalling for the Treatment of Inflammatory Diseases." Cellular Physiology and Biochemistry 49, no. 1 (2018): 349–58. http://dx.doi.org/10.1159/000492885.

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Interleukin (IL)-33, a member of the IL-1 family of cytokines, is involved in innate and adaptive immune responses via interaction with its receptor, ST2. Activation of ST2 signalling by IL-33 triggers pleiotropic immune functions in multiple ST2-expressing immune cells, including macrophages, neutrophils, eosinophils, basophils, mast cells, type 2 helper T cells, regulatory T cells, and group 2 innate lymphoid cells. IL-33-mediated effector functions contribute to the tissue inflammatory and reparative responses in various organs including lung, skin, kidney, central nerve system, cardiovascu

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Liu, Quan, Jeremy M. Lott, Lisa R. Mathews, et al. "IL-33-Driven Innate Tissue-Protective Function of ST2+ Treg Cells." Journal of Immunology 196, no. 1_Supplement (2016): 51.7. http://dx.doi.org/10.4049/jimmunol.196.supp.51.7.

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Abstract Non-lymphoid tissue-resident CD4+ Foxp3+ regulatory T (Treg) cells with the capacity to modulate non-immunological processes including organismal metabolism and tissue repair have been recently described. Notably, a large fraction of non-lymphoid tissue-resident Treg cells express ST2, the receptor for the tissue-derived cytokine and alarmin, IL-33. However, the relationship between IL-33 and ST2+ Treg cells in quiescent and pathogenic states is only starting to be understood. Using FACS and Foxp3 reporter mice, we demonstrate that ST2+ Treg cells from naïve animals are phenotypically

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Wang, Xuan, Xiaoqing Shao, Xinhao Liu, Qiu Qin, Jian Xu, and Jin A. Zhang. "Dysregulated Interleukin -33/ST2 Pathway Perpetuates Chronic Inflammation in Hashimoto’s Thyroiditis." Endocrine, Metabolic & Immune Disorders - Drug Targets 19, no. 7 (2019): 1012–21. http://dx.doi.org/10.2174/1871530319666190226164309.

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Objective: Hashimoto’s Thyroiditis (HT) is an autoimmune disease, characterized by chronic inflammation of the thyroid gland with unknown etiologies. Recently, interleukin-33/ST2 (IL- 33/ST2) pathway reveals its participation in the process of several autoimmune diseases. In this study, the role of IL-33/ST2 pathway in the development of HT is investigated. Methods: The levels of plasma IL-33, sST2 and the frequency of circulating CD4+ST2L+T cells in 30 HT patients and 20 healthy controls were determined by enzyme-linked immunosorbent assay (ELISA) and flow cytometry respectively. The mRNA exp

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Liu, Caini, Jianxin Xiao, and Wen Qian. "A method for in vitropolarization of pathogenic ST2-expressing memory Th2 cells." Journal of Immunology 210, no. 1_Supplement (2023): 64.09. http://dx.doi.org/10.4049/jimmunol.210.supp.64.09.

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Abstract IL-33 and its receptor subunit ST2 (IL1RL1) have been linked to type 2 eosinophilic asthma in multiple human and mouse studies. In particular, recent clinical trials demonstrate that monoclonal antibodies targeting IL-33/ST2 are beneficial to subsets of asthma patients. ST2 +memory Th2 cells (mTh2) are important effector cells in IL-33-mediated type 2 eosinophilic asthma. Herein we describe a unique method for polarizing a subset of pathogenic ST2 +mTh2 (ST2 +mTh2p) cells from naïve mouse CD4 T cells in vitro, which does not require multi-round activation/resting or co-culturing with

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Roessing, Anna, Aravind Cherukuri, David Rothstein, and Heth Roderick Turnquist. "Foxp3+ regulatory T cell expression of IL-10 is required for IL-33-mediated expansion of regulatory B cells." Journal of Immunology 198, no. 1_Supplement (2017): 80.13. http://dx.doi.org/10.4049/jimmunol.198.supp.80.13.

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Abstract BACKGROUND FoxP3+ regulatory T cells (Tregs) are crucial to self- and antigen-specific tolerance. IL-33 drives expansion of Tregs expressing the IL-33 receptor, ST2, and secreting high levels of IL-10. Regulatory B cells (Bregs) are recently identified negative regulators of the immune system and depend on IL-10 to suppress effector T cell responses. In new data, we find that IL-33 also expands Bregs, however, the relationship between ST2+ Treg and Bregs cells remains unknown. Herein we elucidated if a directional relationship exists between IL-33-expanded Bregs and Tregs. METHODS B6

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Ohno, Tatsukuni, Susumu Nakae, and Miyuki Azuma. "Paracrine IL-33 stimulation enhances lipopolysaccharide-mediated macrophage activation (117.30)." Journal of Immunology 186, no. 1_Supplement (2011): 117.30. http://dx.doi.org/10.4049/jimmunol.186.supp.117.30.

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Abstract BACKGROUND: IL-33, a member of the IL-1 family of cytokines, provokes Th2-type inflammation accompanied by accumulation of eosinophils through IL-33R, which consists of ST2 and IL-1RAcP. We previously demonstrated that macrophages produce IL-33 in response to LPS. Some immune responses were shown to differ between ST2-deficient mice and soluble ST2-Fc fusion protein-treated mice. Even in anti-ST2 antibody (Ab)-treated mice, the phenotypes differed between distinct Ab clones, because the characterization of such Abs (i.e., depletion, agonistic or blocking Abs) was unclear in some cases

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Reichenbach, Dawn K., Vincent Schwarze, Benjamin M. Matta, et al. "Regulation of Immune Responses during Acute GvHD Via the IL-33/ST2 Axis." Blood 124, no. 21 (2014): 844. http://dx.doi.org/10.1182/blood.v124.21.844.844.

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Abstract The IL-1 superfamily member IL-33 is produced in barrier tissues. IL-33 binds to the receptor suppression of tumorigenicity 2 (ST2), expressed on stromal cells, regulatory T cells (Tregs), myeloid derived suppressor cells (MDSCs), and macrophages. IL-33 has both anti-inflammatory and pro-inflammatory properties. It is not known if IL-33 plays a role in acute GvHD, and if so what properties it exerts. By immunohistochemistry staining of gut tissues, IL-33 production by non-hematopoietic cells was increased in mice post-conditioning and in patients during GvHD. To determine whether IL-3

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Tonacci, Alessandro, Paolina Quattrocchi, and Sebastiano Gangemi. "IL33/ST2 Axis in Diabetic Kidney Disease: A Literature Review." Medicina 55, no. 2 (2019): 50. http://dx.doi.org/10.3390/medicina55020050.

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Interleukin-33 (IL-33) is a cytokine belonging to the IL-1 family, playing a role in inflammatory, infectious and autoimmune diseases and expressed in the cellular nucleus in several tissues. High levels of IL-33 are expressed in epithelial barrier tissues and endothelial barriers. ST2 is a receptor for IL-33, expressed selectively on a subset of Th2 cells, mediating some of their functions. The IL-33/ST2 axis plays an important role in several acute and chronic inflammatory diseases, including asthma and rheumatoid arthritis. Different disorders are related to the activity of IL-33, ST2, or t

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Mathias, Clinton B., Dylan Krajewski, Marcela T. Taruselli, et al. "Interleukin-10 enhances IL-33-mediated MC activation and modulates the development of food allergy." Journal of Immunology 208, no. 1_Supplement (2022): 49.11. http://dx.doi.org/10.4049/jimmunol.208.supp.49.11.

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Abstract We recently demonstrated an unexpected, proinflammatory role for the pleiotropic cytokine, IL-10, in promoting mast cell (MC) responses during food allergy. IL-10 enhanced MC proliferation and survival and promoted IgE-dependent responses to enteric ovalbumin (OVA) challenge. However, whether the effects of IL-10 on MCs extend beyond IgE-mediated signaling is not clear. To determine whether IL-10 can prime MC activation mediated by IgE-independent stimuli, we assessed the effects of rIL-10 on IL-33-stimulated bone marrow-derived MCs (BMMCs) and examined the development of food allergy

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Rostan, Octavie, Muhammad Imran Arshad, Claire Piquet-Pellorce, Florence Robert-Gangneux, Jean-Pierre Gangneux, and Michel Samson. "Crucial and Diverse Role of the Interleukin-33/ST2 Axis in Infectious Diseases." Infection and Immunity 83, no. 5 (2015): 1738–48. http://dx.doi.org/10.1128/iai.02908-14.

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Interleukin-33 (IL-33) has now emerged as a cytokine with diverse and pleiotropic functions in various infectious and inflammatory diseases. IL-33 is expressed by epithelial cells, endothelial cells, fibroblasts, and hepatocytes. The target cells of IL-33 are Th2 cells, basophils, dendritic cells, mast cells, macrophages, NKT cells, and nuocytes, newly discovered natural helper cells/innate lymphoid cells bearing the ST2 receptor. IL-33 has dual functions, both as a traditional cytokine and as a nuclear factor that regulates gene transcription. IL-33 functions as an “alarmin” released followin

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Atamas, Sergei, Edward Pickering, Pavel Kopach, et al. "Full-length IL-33 acts differently from mature IL-33 in vivo partially in an ST2-independent fashion (120.30)." Journal of Immunology 188, no. 1_Supplement (2012): 120.30. http://dx.doi.org/10.4049/jimmunol.188.supp.120.30.

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Abstract IL-33 is a key regulator of inflammation and immunity. It remains controversial whether protease-mediated activation of IL-33 is needed for functional effects. We constructed and validated recombinant adenoviruses for gene delivery of full-length mouse (flm) and mature mouse (mm) (aa 109-266) IL-33 to mouse lungs in vivo. Gene expression was confirmed by RT-Q-PCR and ELISA. Analyses of BAL samples and lung tissues revealed substantial differences between flmIL-33 and mmIL-33. Both isoforms caused pulmonary infiltration and BAL influx of T and B lymphocytes and neutrophils, whereas mmI

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St. Rose, Marie-Clare, Naomi Tsurutani, Adam Adler, and Anthony Vella. "Defining the role of the alarmin IL-33 during the CD8 T cell effector response (VAC3P.958)." Journal of Immunology 192, no. 1_Supplement (2014): 73.20. http://dx.doi.org/10.4049/jimmunol.192.supp.73.20.

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Abstract ST2, the receptor for the alarmin IL-33, is expressed on CD8 T cells and both IL-33 and ST2 can optimize anti-viral CD8 T cell immune responses. Further, signaling through ST2 in combination with innate-derived cytokines such as IL-12 can induce TCR-independent production of IFN-gamma. We sought to understand the role of the IL-33/ST2 pathway during the effector CD8 T cell response elicited after immunization with CD134 and CD137 costimulatory agonists. ST2 is rapidly up-regulated on CD27+ effector CD8 T cells during the earliest phase of T cell re-activation, even before the up-regul

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Aggeletopoulou, Ioanna, Efthymios P. Tsounis, and Christos Triantos. "Molecular Mechanisms Underlying IL-33-Mediated Inflammation in Inflammatory Bowel Disease." International Journal of Molecular Sciences 24, no. 1 (2022): 623. http://dx.doi.org/10.3390/ijms24010623.

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Interleukin-33 (IL-33) is a cytokine defined by its pleiotropic function, acting either as a typical extracellular cytokine or as a nuclear transcription factor. IL-33 and its receptor, suppression of tumorigenicity 2 (ST2), interact with both innate and adaptive immunity and are considered critical regulators of inflammatory disorders. The IL-33/ST2 axis is involved in the maintenance of intestinal homeostasis; on the basis of their role as pro- or anti-inflammatory mediators of first-line innate immunity, their expression is of great importance in regard to mucosal defenses. Mucosal immunity

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Cordero da Luz, Felipe Andrés, Ana Paula Lima Oliveira, Daniella Borges, Paula Cristina Brígido, and Marcelo José Barbosa Silva. "The Physiopathological Role of IL-33: New Highlights in Bone Biology and a Proposed Role in Periodontal Disease." Mediators of Inflammation 2014 (2014): 1–8. http://dx.doi.org/10.1155/2014/342410.

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Interleukin-33 (IL-33) is a recently described member of the IL-1 family. IL-33 acts as an alarmin, chemoattractant, and nuclear factor. ST2, a member of the Toll-like receptor/IL-1R superfamily, the receptor of IL-33, triggers a plethora of downstream effectors and leads the activation of NFK-B, leading the expression of several genes. IL-33 and ST2 are expressed in the majority of cell types, and the IL-33/ST2 axis has a role in immune response, bone homeostasis, and osteoclastogenesis. Several studies show opposite roles of IL-33 in osteoclastogenesis and the implication in bone biology. Fe

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Jovicic, Nemanja, Ilija Jeftic, Marina Miletic Kovacevic, et al. "ST2 Deficiency Ameliorates High Fat Diet-Induced Liver Steatosis In BALB/c Mice." Serbian Journal of Experimental and Clinical Research 16, no. 1 (2015): 9–20. http://dx.doi.org/10.1515/sjecr-2015-0002.

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ABSTRACTNon-alcoholic fatty liver disease (NAFLD) is strongly associated with obesity, but the molecular mechanisms of liver steatosis and its progression to non-alcoholic steatohepatitis and fibrosis are incompletely understood. Immune reactivity plays an important role in the pathogenesis of NAFLD. The IL-33/ST2 axis has a protective role in adiposity and atherosclerosis, but its role in obesity-associated metabolic disorders requires further clarification. To investigate the unresolved role of IL-33/ST2 signalling in NAFLD, we used ST2-deficient (ST2-/-) and wild type (WT) BALB/c mice maint

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Rasheed, Kashif, Ugo Moens, Benedetta Policastro, et al. "The Merkel Cell Polyomavirus T-Antigens and IL-33/ST2-IL1RAcP Axis: Possible Role in Merkel Cell Carcinoma." International Journal of Molecular Sciences 23, no. 7 (2022): 3702. http://dx.doi.org/10.3390/ijms23073702.

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Merkel cell polyomavirus (MCPyV) is a causal factor in Merkel cell carcinoma (MCC). The oncogenic potential is mediated through its viral oncoproteins large T-antigen (LT) and small T-antigen (sT). Cytokines produced by tumor cells play an important role in cancer pathogenesis, and viruses affect their expression. Therefore, we compared human cytokine and receptor transcript levels in virus positive (V+) and virus negative (V−) MCC cell lines. Increased expression of IL-33, a potent modulator of tumor microenvironment, was observed in V+ MCC cell lines when compared to V− MCC-13 cells. Transie

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Mathews, Lisa, Brian Rosborough, Angus Thomson, and Heth Turnquist. "IL-33 directly supports the proliferation of suppressive, naturally-occurring regulatory T cells expressing the IL-33 receptor, ST2 (161.1)." Journal of Immunology 188, no. 1_Supplement (2012): 161.1. http://dx.doi.org/10.4049/jimmunol.188.supp.161.1.

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Abstract Overview: Both IL-33 and its receptor, ST2, have been ascribed T helper type-2 (Th2) response promoting capacities. However, IL-33 increases splenic CD4+ forkhead box P3 (Foxp3)+ regulatory T cells (Treg) and post-transplant IL-33 monotherapy mediates a Treg-dependent prolongation of experimental cardiac allograft survival. As such, we addressed whether IL-33 directly targets Treg to support their expansion or suppressive function. Methods: The ability of recombinant IL-33 to facilitate anti-CD3/CD28-stimulated proliferation of BALB/c St2+/+ or St2-/- CD4+ CD25+ T cells was compared t

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Saju, Blessy, Ryszard Nosalski, Emma Booth, and Tomasz Guzik. "O47 THE ROLE OF IL-33 AND ST2 IN THE MODULATION OF TARGET ORGAN DAMAGE IN ANGIOTENSIN II-DEPENDENT HYPERTENSION." Journal of Hypertension 42, Suppl 3 (2024): e23. http://dx.doi.org/10.1097/01.hjh.0001062652.01841.00.

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Introduction: Hypertension is associated with a chronic inflammatory state and aberrant immune system activity. Interleukin-33/suppression of tumorigenicity 2 (IL-33/ST2) signalling axis is important in the modulation of atherosclerosis and cardiovascular fibrosis. We aimed to evaluate the modulation of IL-33 and ST2 in hypertensive mouse models and patients. Methods and Results: Hypertension was induced by a 14-day infusion of Ang-II (490ng/min/kg) in 12-week-old WT C57BL/6, ST2KO, IL33KO mice. IL-33 and ST2 mRNA and protein were evaluated using qPCR and Western blot in WT mice. Ang II-infusi

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Dwyer, Gaelen K., Lisa Mathews, Amanda H. Lee, et al. "Disruption of IL-33-mediated costimulation to CD4 +T cells leads to peripheral Treg generation and resolution of T cell-mediated pathology." Journal of Immunology 210, no. 1_Supplement (2023): 76.12. http://dx.doi.org/10.4049/jimmunol.210.supp.76.12.

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Abstract Stromal signals are becoming appreciated as critical coordinators of immunity. We recently demonstrated that fibroblastic reticular cell (FRC)-derived IL-33 directly stimulates CD4 +T cells during priming to promote IL-12-independent Type 1 T helper cell (Th1) differentiation and expansion. Utilizing TCR transgenic (Tg) T cells lacking the IL-33 receptor, ST2, we established that IL-33 is a costimulatory molecule augmenting TCR signaling to low affinity or concentration antigens. Blockade of costimulatory molecules can lead to peripheral regulatory T cell (pTreg) induction and our RNA

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Kuo, Chih-Feng, Wei-Yu Chen, Hai-Han Yu, et al. "IL-33/ST2 Axis Plays a Protective Effect in Streptococcus pyogenes Infection through Strengthening of the Innate Immunity." International Journal of Molecular Sciences 22, no. 19 (2021): 10566. http://dx.doi.org/10.3390/ijms221910566.

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Group A Streptococcus (GAS) causes invasive human diseases with the cytokine storm. Interleukin-33 (IL-33)/suppression of tumorigenicity 2 (ST2) axis is known to drive TH2 response, while its effect on GAS infection is unclear. We used an air pouch model to examine the effect of the IL-33/ST2 axis on GAS-induced necrotizing fasciitis. GAS infection induced IL-33 expression in wild-type (WT) C57BL/6 mice, whereas the IL-33- and ST2-knockout mice had higher mortality rates, more severe skin lesions and higher bacterial loads in the air pouches than those of WT mice after infection. Surveys of in

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Pastille, Eva, Marie-Hélène Wasmer, Alexandra Adamczyk, et al. "The IL-33/ST2 pathway shapes the regulatory T cell phenotype to promote intestinal cancer." Mucosal Immunology 12, no. 4 (2019): 990–1003. http://dx.doi.org/10.1038/s41385-019-0176-y.

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AbstractThe composition of immune infiltrates strongly affects the prognosis of patients with colorectal cancer (CRC). Interleukin (IL)-33 and regulatory T cells (Tregs) in the tumor microenvironment have been separately implicated in CRC; however their contribution to intestinal carcinogenesis is still controversial. Here, we reveal that IL-33 signaling promotes CRC by changing the phenotype of Tregs. In mice with CRC, tumor-infiltrating Tregs preferentially upregulate IL-33 receptor (ST2), and IL-33/ST2 signaling positively correlates with tumor number and size. Transcriptomic and flow cytom

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Ramirez-Carrozzi, Vladimir, Amy Dressen, Patrick Lupardus, Brian Yaspan, and Rajita Pappu. "Functional analysis of protective IL1RL1 variants associated with asthma risk (CCR6P.215)." Journal of Immunology 194, no. 1_Supplement (2015): 187.2. http://dx.doi.org/10.4049/jimmunol.194.supp.187.2.

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Abstract GWAS studies have identified polymorphisms in both IL33 and IL1RL1, the gene encoding ST2, the high affinity chain of the IL-33 receptor, that associate with asthma susceptibility. We identified amino acid changing variants in IL1RL1 associating with asthma incidence and found these SNPs to be protective from asthma risk in our study population. These variants result in coding changes to the intracellular region of ST2, which contains the TIR domain of the receptor that is critical for signaling downstream of IL-1 cytokine family and TLRs. Mutations or deletions to this region can inh

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Qian, Yujing, and Meifen Zhang. "The Functional Roles of IL-33/ST2 Axis in Ocular Diseases." Mediators of Inflammation 2020 (August 18, 2020): 1–11. http://dx.doi.org/10.1155/2020/5230716.

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Interleukin-33 (IL-33), an important member of the IL-1 family, plays a pivotal role in regulating immune responses via combining with its receptor suppression of tumorigenicity 2 (ST2). We have already known IL-33/ST2 axis participates in the pathogenesis of various diseases, including liver diseases, renal diseases, and neurological diseases. Recently, emerging studies are indicating that IL-33/ST2 is also involved in a wide range of ocular diseases, such as allergic eye disease, keratitis and corneal regeneration, dry eye disease, uveitis, vitreoretinal diseases, and neuromyelitis optica sp

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Hasan, Amal, Shihab Kochumon, Ebaa Al-Ozairi, Jaakko Tuomilehto, and Rasheed Ahmad. "Association between Adipose Tissue Interleukin-33 and Immunometabolic Markers in Individuals with Varying Degrees of Glycemia." Disease Markers 2019 (April 3, 2019): 1–16. http://dx.doi.org/10.1155/2019/7901062.

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Introduction. Interleukin-33 (IL-33), the ligand for the receptor ST2, is abundant in adipose tissue, including preadipocytes, adipocytes, and endothelial cells. The IL-33/ST2 axis is protective against obesity, insulin resistance, and type 2 diabetes (T2D) in animal models. We determined whether adipose tissue IL-33 was associated with glycated hemoglobin (HbA1c), as well as mediators of inflammation and immune regulation and beiging of adipose tissue, among individuals with varying degrees of glycemia. Materials and Methods. A total of 91 adults with normoglycemia, prediabetes, and T2D were

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Liu, Boyi, Yan Tai, Satyanarayana Achanta, et al. "IL-33/ST2 signaling excites sensory neurons and mediates itch response in a mouse model of poison ivy contact allergy." Proceedings of the National Academy of Sciences 113, no. 47 (2016): E7572—E7579. http://dx.doi.org/10.1073/pnas.1606608113.

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Poison ivy-induced allergic contact dermatitis (ACD) is the most common environmental allergic condition in the United States. Case numbers of poison ivy ACD are increasing due to growing biomass and geographical expansion of poison ivy and increasing content of the allergen, urushiol, likely attributable to rising atmospheric CO2. Severe and treatment-resistant itch is the major complaint of affected patients. However, because of limited clinical data and poorly characterized models, the pruritic mechanisms in poison ivy ACD remain unknown. Here, we aim to identify the mechanisms of itch in a

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Abd Rachman Isnadi, Mohammad Faruq, Voon Kin Chin, Roslaini Abd Majid, et al. "Critical Roles of IL-33/ST2 Pathway in Neurological Disorders." Mediators of Inflammation 2018 (2018): 1–9. http://dx.doi.org/10.1155/2018/5346413.

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Interleukin-33 (IL-33) is an IL-1 family member, which exhibits both pro- and anti-inflammatory properties solely based on the type of the disease itself. Generally, IL-33 is expressed by both endothelial and epithelial cells and mediates its function based on the interaction with various receptors, mainly with ST2 variants. IL-33 is a potent inducer for the Th2 immune response which includes defence mechanism in brain diseases. Thus, in this paper, we review the biological features of IL-33 and the critical roles of IL-33/ST2 pathway in selected neurological disorders including Alzheimer’s di

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Caselli, C., A. D'Amico, R. Ragusa, et al. "IL-33/ST2 Pathway and Classical Cytokines in End-Stage Heart Failure Patients Submitted to Left Ventricular Assist Device Support: A Paradoxic Role for Inflammatory Mediators?" Mediators of Inflammation 2013 (2013): 1–9. http://dx.doi.org/10.1155/2013/498703.

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Background. Inflammation is a critical process contributing to heart failure (HF). We hypothesized that IL-33/ST2 pathway, a new mechanism regulated during cardiac stress, may be involved in the functional worsening of end-stage HF patients, candidates for left ventricular assist device (LVAD) implantation, and potentially responsible for their outcome.Methods. IL-33, ST2, and conventional cytokines (IL-6, IL-8, and TNF-α) were determined in cardiac biopsies and plasma of 22 patients submitted to LVAD implantation (pre-LVAD) and compared with (1) control stable chronic HF patients on medical t

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Zhou, Ju, Ting Zhuang, Peng Ma, et al. "MicroRNA-547-5p-mediated interleukin-33/suppressor of tumorigenicity 2 signaling underlies the genesis and maintenance of neuropathic pain and is targeted by the therapy with bone marrow stromal cells." Molecular Pain 16 (January 2020): 174480692093173. http://dx.doi.org/10.1177/1744806920931737.

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Interleukin-33 (IL-33)/suppressor of tumorigenicity 2 (ST2) signaling is known to promote inflammation and the genesis and maintenance of neuropathic pain. However, it remained mostly unknown how IL-33/ST2 signaling can be enhanced by neuropathic stimulations. Here, we report that the chronic constriction nerve injury (CCI)-induced increases in the expression of IL-33 and ST2 and a decrease in microRNA (miRNA)-547-5p not only in the dorsal root ganglia (DRG) but also in spinal dorsal horn (SDH) ipsilateral to the CCI. We found that increasing endogenous miRNA-547-5p by the intrathecal (i.t.) i

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Chen, Wei-Yu, Jaewoo Hong, Joseph Gannon, Rahul Kakkar, and Richard T. Lee. "Myocardial pressure overload induces systemic inflammation through endothelial cell IL-33." Proceedings of the National Academy of Sciences 112, no. 23 (2015): 7249–54. http://dx.doi.org/10.1073/pnas.1424236112.

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Hypertension increases the pressure load on the heart and is associated with a poorly understood chronic systemic inflammatory state. Interleukin 33 (IL-33) binds to membrane-bound ST2 (ST2L) and has antihypertrophic and antifibrotic effects in the myocardium. In contrast, soluble ST2 appears to act as a decoy receptor for IL-33, blocking myocardial and vascular benefits, and is a prognostic biomarker in patients with cardiovascular diseases. Here we report that a highly local intramyocardial IL-33/ST2 conversation regulates the heart’s response to pressure overload. Either endothelial-specifi

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Gombert, Jean-Marc, Anaïs Levescot, Stéphane Flamant, et al. "Bcr/Abl-induced deregulation of the IL-33/ST2 pathway in CD34(+) progenitors from chronic myeloid leukemia patients (P6284)." Journal of Immunology 190, no. 1_Supplement (2013): 46.13. http://dx.doi.org/10.4049/jimmunol.190.supp.46.13.

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Abstract Although it is generally acknowledged that cytokines regulate normal hematopoiesis in an autocrine/paracrine fashion, their possible role in chronic myeloid leukemia (CML) and resistance to imatinib mesylate (IM) treatment remain poorly investigated. Here, we report that CD34(+) progenitors from CML patients at diagnosis are selectively targeted by the cytokine/alarmin IL-33. Indeed, CML CD34(+) progenitors up-regulate their cell surface expression of the IL-33-specific receptor chain ST2, proliferate and produce cytokines in response to IL-33, conversely to CD34(+) cells from healthy

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Choi, Yeon-Sook, Hyun-Jung Choi, Jeong-Ki Min, et al. "Interleukin-33 induces angiogenesis and vascular permeability through ST2/TRAF6-mediated endothelial nitric oxide production." Blood 114, no. 14 (2009): 3117–26. http://dx.doi.org/10.1182/blood-2009-02-203372.

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Interleukin-33 (IL-33), a member of the IL-1 cytokine family, is emerging as a new regulator of immune responses and inflammatory vascular diseases. Although IL-33 and its cognate receptor ST2 appear to be expressed in vascular cells, the precise role of IL-33 in the vasculature has not been determined. In this study, we report a novel role of IL-33 as a potent endothelial activator, promoting both angiogenesis and vascular permeability. IL-33 increased proliferation, migration, and morphologic differentiation of human endothelial cells, consistently with increased angiogenesis in vivo. IL-33

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Reichenbach, Dawn K., Vincent Schwarze, Benjamin M. Matta, et al. "The IL-33/ST2 axis augments effector T-cell responses during acute GVHD." Blood 125, no. 20 (2015): 3183–92. http://dx.doi.org/10.1182/blood-2014-10-606830.

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Key Points IL-33 and ST2 expression are increased post-conditioning and with GVHD, resulting in increased T-cell activation via the IL-33/ST2 axis. Infusion of ST2-Fc protein exploits sST2’s function as a negative regulator of acute GVHD inhibiting pro-inflammatory cytokines.

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Yang, Fuhan, Mingming Wen, Dayu Pan, et al. "IL-33/ST2 Axis Regulates Vasculogenic Mimicry via ERK1/2-MMP-2/9 Pathway in Melanoma." Dermatology 235, no. 3 (2019): 225–33. http://dx.doi.org/10.1159/000498857.

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Background: Melanoma, an extremely malignant form of cancer, poses a significant health risk. Vasculogenic mimicry (VM), blood vessels formed by tumor cells instead of endothelial cells, is an important factor for the rapid progression of melanoma. Interleukin (IL)-33 is an inflammatory factor commonly found in the tumor microenvironment and plays an important role in the progression of many tumors. IL-33 acts on immune cells and tumor cells through its receptor ST2. This study hypothesized that IL-33 directly affects the progression of melanoma. Objectives: This study was designed to investig

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Leal-Silva, Thaís, Flaviane Vieira-Santos, Fabrício Marcus Silva Oliveira, et al. "Detrimental role of IL-33/ST2 pathway sustaining a chronic eosinophil-dependent Th2 inflammatory response, tissue damage and parasite burden during Toxocara canis infection in mice." PLOS Neglected Tropical Diseases 15, no. 7 (2021): e0009639. http://dx.doi.org/10.1371/journal.pntd.0009639.

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Toxocariasis is a neglected disease that affects people around the world. Humans become infected by accidental ingestion of eggs containing Toxocara canis infective larvae, which upon reaching the intestine, hatch, penetrate the mucosa and migrate to various tissues such as liver, lungs and brain. Studies have indicated that Th2 response is the main immune defense mechanism against toxocariasis, however, there are still few studies related to this response, mainly the IL-33/ST2 pathway. Some studies have reported an increase in IL-33 during helminth infections, including T. canis. By binding t

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Wierzbicka, Justyna M., Anna Piotrowska, Dorota Purzycka-Bohdan, et al. "The Effects of Vitamin D on the Expression of IL-33 and Its Receptor ST2 in Skin Cells; Potential Implication for Psoriasis." International Journal of Molecular Sciences 22, no. 23 (2021): 12907. http://dx.doi.org/10.3390/ijms222312907.

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Interleukin 33 (IL-33) belongs to the IL-1 family and is produced constitutively by epithelial and endothelial cells of various organs, such as the skin. It takes part in the maintenance of tissue homeostasis, repair, and immune response, including activation of Th2 lymphocytes. Its involvement in pathogenesis of several inflammatory diseases including psoriasis was also suggested, but this is not fully understood. The aim of the study was to investigate expression of IL-33 and its receptor, ST2, in psoriasis, and the effects of the active form of vitamin D (1,25(OH)2D3) on their expression in

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Noel, Gregory, Muhammad Imran Arshad, Aveline Filliol, et al. "Ablation of interaction between IL-33 and ST2+ regulatory T cells increases immune cell-mediated hepatitis and activated NK cell liver infiltration." American Journal of Physiology-Gastrointestinal and Liver Physiology 311, no. 2 (2016): G313—G323. http://dx.doi.org/10.1152/ajpgi.00097.2016.

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The IL-33/ST2 axis plays a protective role in T-cell-mediated hepatitis, but little is known about the functional impact of endogenous IL-33 on liver immunopathology. We used IL-33-deficient mice to investigate the functional effect of endogenous IL-33 in concanavalin A (Con A)-hepatitis. IL-33−/− mice displayed more severe Con A liver injury than wild-type (WT) mice, consistent with a hepatoprotective effect of IL-33. The more severe hepatic injury in IL-33−/− mice was associated with significantly higher levels of TNF-α and IL-1β and a larger number of NK cells infiltrating the liver. The ex

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Wang, Jun-Xia, Shinjiro Kaieda, and Peter Nigrovic. "IL-33/ST2 promotes tissue mastocytosis under conditions of inflammation (CCR3P.219)." Journal of Immunology 192, no. 1_Supplement (2014): 115.16. http://dx.doi.org/10.4049/jimmunol.192.supp.115.16.

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Abstract Mast cells (MC) are potent innate immune cells that accumulate in chronically inflamed tissues, where they have been implicated in multiple allergic and inflammatory diseases. MC express the IL-33 receptor ST2, and this new member of the IL-1 cytokine family is recognized as an important pathway both for direct MC activation and for priming MC to respond to other pro-inflammatory signals. However, IL-33 has no known role in tissue mastocytosis. Using primary MC cultured from human skin, we found that IL-33 did not alter MC proliferation but instead protected MC from apoptosis, princip

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Maggi, Laura, Genil Mororó Araújo Camelo, Izabella Chrystina Rocha, et al. "Role of the IL-33/ST2 Activation Pathway in the Development of the Hepatic Fibrosis Induced by Schistosoma mansoni Granulomas in Mice." International Journal of Molecular Sciences 24, no. 12 (2023): 10237. http://dx.doi.org/10.3390/ijms241210237.

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Schistosoma mansoni eggs retained in host tissues induce innate cytokine release, contributing to the induction of Type-2 immune responses and granuloma formation, important to restrain cytotoxic antigens, but leading to fibrosis. Interleukin(IL)-33 participates in experimental models of inflammation and chemically induced fibrosis, but its role in S. mansoni-induced fibrosis is still unknown. To explore the role of the IL-33/suppressor of the tumorigenicity 2 (ST2) pathway, serum and liver cytokine levels, liver histopathology, and collagen deposition were comparatively evaluated in S. manson

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