The ST2 is a member of family of receptors of interleukin I (IL-I) and consists of two isoforms: a trans-membrane of cellular one (ST2L) and soluble or circulating one (sST2). The ST2 is a receptor of IL-33 that represents IL-I like cytokine. The IL-33 manifests its cellular functions binding receptor complex consisted of accessory protein ST2L and IL-IR. The system IL-33/ST2 is activated in cardiomyocytes and fibroblasts in response to mechanical irritation or damage. It was demonstrated that interaction between IL-33 and ST2L is a cardioprotective one. The experimental models were used to demonstrate decreasing of myocardium fibrosis, prevention of development of hypertrophy of cardiomyocytes, decreasing of apoptosis and amelioration of functional capacity of myocardium at interaction of IL-33 and ST2L. In particular, the positive effects of IL-33 are related to receptor of ST2L. In turn, sST2 by binding with IL-33 sets blocking of interaction between IL-33/ST2L hence eliminating cardioprotective effects. During last years, the knowledge about the role of ST2 in pathophysiology of cardio-vascular diseases broadened and now the role of ST2 is related to myocardium dysfunction, fibrosis and remodeling. The system IL-33/ST2L, besides its myocardial role, can play an additional role in development and progressing of atherosclerosis. The system IL-33/ST2L can have a therapeutic potential in case of myocardial overload or trauma. On the contrary, sST2 acts as a false receptor of IL-33 blocking cardioprotective effects of interaction of IL-33/ST2L.
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http://dx.doi.org/10.18821/0869-2084-2017-62-10-599-605 | DOI Listing |
Expert Opin Emerg Drugs
January 2025
Department of Medical and Surgical Sciences, University "Magna Græcia" of Catanzaro - Catanzaro, Italy.
Introduction: Severe asthma is a chronic airway disease characterized by many pathomechanisms known as endotypes. Biological therapies targeting severe asthma endotypes have significantly improved the treatment of this disease, thus remarkably bettering patient quality of life.
Areas Covered: This review aims to describe current biological therapies for severe asthma, highlighting emerging ones.
Allergy
January 2025
Department of Pediatrics and Adolescent Medicine, Juntendo University Graduate School of Medicine, Tokyo, Japan.
Background: IgE-mediated food allergy is accompanied by mucosal mast cell (MMC) hyperplasia in the intestinal mucosa. Intestinal MMC numbers correlate with the severity of food allergy symptoms. However, the mechanisms by which MMCs proliferate excessively are poorly understood.
View Article and Find Full Text PDFJ Allergy Clin Immunol
January 2025
Departments of Animal Science, Integrative Biology and Physiology, University of Minnesota,St. Paul, MN, 55108. Electronic address:
Background: Environmental allergens induce the release of danger signals from the airway epithelium that trigger type 2 immune responses and promote airway inflammation.
Objective: To investigate the role of allergen-stimulated P2Y receptor activation in regulating ATP, IL-33 and DNA release by human bronchial epithelial (hBE) cells and mouse airways.
Methods: hBE cells were exposed to Alternaria alternata extract and secretion of ATP, IL-33 and DNA were studied in vitro.
J Allergy Clin Immunol
January 2025
Division of Allergy, Asthma and Clinical Immunology, Mayo Clinic, Scottsdale, Ariz; Department of Medicine, Mayo Clinic, Scottsdale, Ariz; Department of Immunology, Mayo Clinic Rochester, Rochester, Minn; Department of Immunology, Mayo Clinic Arizona, Scottsdale, Ariz.
Over the past two decades, mechanistic studies of allergic and type 2 (T2)-mediated airway inflammation have led to multiple approved therapies for the treatment of moderate-to-severe asthma. The approval and availability of these monoclonal antibodies targeting immunoglobulin E, a type 2 cytokine (IL-5) and/or cytokine receptors (IL-5Rα, IL-4Rα) has been central to the progresses made in the management of moderate-to-severe asthma over this period. However, there are persistent gaps in clinician's ability to provide precise care given that many patients with type 2-high asthma do not respond to the IgE or T2 cytokine-targeting therapies and patients with type 2-low asthma have limited therapeutic options.
View Article and Find Full Text PDFCurr Cardiol Rev
January 2025
Department of Pharmacy, Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Moradabad (UP)-244001, India.
Cardiovascular diseases remain a significant reason for illness and death globally. Although certain interleukins have been extensively researched about cardiovascular disease (CVD), new findings have identified unique members of the interleukin family that could potentially play a role in cardiovascular well-being and ailments. This review discusses the current understanding of the role of these recently identified interleukins, such as IL-27, IL-31, IL-32, IL-33, and the IL-28 group (IL-28A, IL-28B, IL-29), in the development of cardiovascular diseases.
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