Relevant bibliographies by topics / ST2/IL-33

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  1. Journal articles
  2. Dissertations / Theses
  3. Book chapters
  4. Conference papers

Academic literature on the topic 'ST2/IL-33'

Author: Grafiati
Published: 9 March 2023
Last updated: 31 July 2025

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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 (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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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’
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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 w
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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
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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 activati
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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.

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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 n
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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.

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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 t
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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 r
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Tariq, Mubashira. "IL-33/ST2 and tissue Treg/AREG pathways in the pathophysiology of HIV infection." Electronic Thesis or Diss., Paris 12, 2021. http://www.theses.fr/2021PA120017.

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Depuis les thérapies antirétrovirales (ART), les principales causes de mortalité et de morbidité sont liées à des pathologies non liées aux SIDA qui sont dûes à un niveau d’inflammation chronique de bas bruit. Cette inflammation est liée entre autre à la persistance de la perte d’homéostasie intestinale qui conduit à des translocations microbiennes dans la circulation systémique. En effet, les sujets traités et infectés par le VIH présentent une déplétion sévère et massive des lymphocytes T CD4+, en particulier dans le tissu lymphoïde associé à l'intestin (GALT) une altération de la barrière é
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Fanny, Manoussa. "Etude des mécanismes de l’inflammation pulmonaire lors de l’exposition aux nanoparticules ou la fumée de cigarette : implication des voies de signalisations des récepteurs ST2 et NLRP6." Thesis, Orléans, 2016. http://www.theses.fr/2016ORLE2057/document.

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Les maladies pulmonaires, responsables de 3,1 millions de décès de part le monde représentent un problème majeur de santé publique. En particulier, la fibrose pulmonaire et la broncho-pneumopathie chronique obstructive (BPCO) conduisent à la perte de la fonction pulmonaire. Aucun traitement efficace n’a été identifié à ce jour pour lutter contre ces maladies, la seule alternative étant la transplantation. Au cours de ma thèse, j’ai exploré les mécanismes du développement de ces maladies en utilisant différents modèles chez la souris, soit par l’instillation de nanoparticules de métaux ou de bl
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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. Editora Creative, 2021. http://dx.doi.org/10.53924/pswr.04.

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Conference 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). Atlantis Press, 2018. http://dx.doi.org/10.2991/meici-18.2018.98.

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Cohen, Suzanne, Ian Scott, Jayesh Majithiya, 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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Asrat, S., Y. Mao, Y. Zhou, et al. "Itepekimab Binds to IL-33 With High Affinity, Prevents the Formation of IL-33/ST2/IL-1RAcP Signaling Complex and Blocks Mediators of Airway Inflammation." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a4478.

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Yu, S. L., Y. B. Huo, C. H. Huang, 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, 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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Andersson, Cecilia, Premkumar Siddhuraj, Caroline Sandén, et al. "COPD patients display pronounced changes of IL-33 and ST2 expression in alveolar capillary phenotypes." In ERS Congress 2024 abstracts. European Respiratory Society, 2024. http://dx.doi.org/10.1183/13993003.congress-2024.oa1071.

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