Document Detail


Interleukin-1 receptor antagonist (IL-1Ra) and IL-1Ra producing mesenchymal stem cells as modulators of diabetogenesis.
MedLine Citation:
PMID:  19845478     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The increase of pro-inflammatory cytokines and oxidative stress leads to beta-cell damage and promotes beta-cells apoptosis, in types I and II of diabetes mellitus. Therefore, blocking of pro-inflammatory cytokines should be an effective way for the treatment of diabetes mellitus. When IL-1 occupies its receptor, various pro-inflammatory events are initiated including the synthesis and releases of chemokines and these chemokines attract neutrophils, macrophages, and lymphocytes that cause tissue inflammation. IL-1Ra is a naturally occurring cytokine and is the inhibitor of IL-1. When IL-1Ra binds to the IL-1 receptor, binding of IL-1 is blocked by IL-1Ra and pro-inflammatory signal from IL-1 receptor is stopped. There are mounting evidences to suggest that anti-inflammatory IL-1Ra reduces the inflammatory effects of IL-1 and preserves cell function in both types of diabetes. Therefore, IL-1Ra maybe a new therapeutic agent for diabetes mellitus types I and II. Mesenchymal stem cells (MSCs) are self-renewable multipotent stromal cells that have immunomodulatory capacity. Recently, well characterized subpopulations of MSCs which express IL-1Ra have been described. IL-1Ra expressed by these MSCs effectively binds to IL-1 receptor and protects tissues from inflammation-induced injuries. It has been previously shown that bone marrow-derived MSC therapy could be considered for the treatment of diabetes mellitus type 1 and complications of diabetes mellitus. This review presents understanding of potential use of IL-1Ra and MSCs as modulators of diabetogenesis.
Authors:
Vladislav Volarevic; Ahmed Al-Qahtani; Nebojsa Arsenijevic; Sladjana Pajovic; Miodrag L Lukic
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Autoimmunity     Volume:  43     ISSN:  1607-842X     ISO Abbreviation:  Autoimmunity     Publication Date:  2010 Jun 
Date Detail:
Created Date:  2010-05-14     Completed Date:  2010-08-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8900070     Medline TA:  Autoimmunity     Country:  England    
Other Details:
Languages:  eng     Pagination:  255-63     Citation Subset:  IM    
Affiliation:
Faculty of Medicine, Center for Molecular Medicine, University of Kragujevac, Kragujevac, Serbia.
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MeSH Terms
Descriptor/Qualifier:
Animals
Clinical Trials as Topic
Diabetes Mellitus, Type 1 / prevention & control,  therapy*
Diabetes Mellitus, Type 2 / prevention & control,  therapy*
Humans
Interleukin 1 Receptor Antagonist Protein / metabolism,  therapeutic use*
Interleukin-1 / antagonists & inhibitors,  metabolism
Mesenchymal Stem Cells / metabolism*
Mice
Receptors, Interleukin-1 / metabolism
Treatment Outcome
Chemical
Reg. No./Substance:
0/Interleukin 1 Receptor Antagonist Protein; 0/Interleukin-1; 0/Receptors, Interleukin-1

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