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Blockade of interleukin 1 in type 1 diabetes mellitus

Mandrup-Poulsen, Thomas and Pickersgill, Linda and Donath, Marc Yves. (2010) Blockade of interleukin 1 in type 1 diabetes mellitus. Nature Reviews. Endocrinology, Vol. 6, no. 3. pp. 158-166.

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Official URL: http://edoc.unibas.ch/dok/A6007277

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Abstract

Interleukin 1 (IL-1) is a 17 kDa protein highly conserved through evolution and is a key mediator of inflammation, fever and the acute-phase response. IL-1 has important functions in the innate immune defense against microbes, trauma and stress, and is also an effector molecule involved in tissue destruction and fibrosis. The inhibition of IL-1 action has clinical efficacy in many inflammatory diseases, such as hereditary autoinflammatory disorders, familial hereditary fever, gout, rheumatoid arthritis and type 2 diabetes mellitus (T2DM). The latter is a common metabolic condition caused by insulin resistance and pancreatic beta-cell failure, the causes of both of which have inflammatory components. IL-1 signaling has roles in beta-cell dysfunction and destruction via the NFkappaB and mitogen-activated-protein-kinase pathways, leading to endoplasmic reticulum and mitochondrial stress and eventually activating the apoptotic machinery. In addition, IL-1 acts on T-lymphocyte regulation. The modulating effect of IL-1 on the interaction between the innate and adaptive immune systems and the effects of IL-1 on the beta-cell point to this molecule being a potential interventional target in autoimmune diabetes mellitus. Genetic or pharmacological abrogation of IL-1 action reduces disease incidence in animal models of type 1 diabetes mellitus (T1DM) and clinical trials have been started to study the feasibility, safety and efficacy of IL-1 therapy in patients with T1DM. Here, we review the rationale for blocking IL-1 in patients with T1DM.
Faculties and Departments:03 Faculty of Medicine > Departement Biomedizin > Department of Biomedicine, University Hospital Basel > Infection Biology (Khanna)
UniBasel Contributors:Donath, Marc
Item Type:Article, refereed
Article Subtype:Further Journal Contribution
Bibsysno:Link to catalogue
Publisher:Nature Publishing Group
ISSN:1759-5029
Note:Publication type according to Uni Basel Research Database: Journal item
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Last Modified:16 Aug 2013 07:34
Deposited On:16 Aug 2013 07:31

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