Document Detail


Transgenic expression of survivin compensates for OX40-deficiency in driving Th2 development and allergic inflammation.
MedLine Citation:
PMID:  23616302     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Survivin, an inhibitor of apoptosis family molecule, has been proposed as a crucial intermediate in the signaling pathways leading to T-cell development, proliferation, and expansion. However, the importance of survivin to T-cell-driven inflammatory responses has not been demonstrated. Here, we show that survivin transgenic mice exhibit an increased antigen-driven Th2 lung inflammation and that constitutive expression of survivin reversed the defective lung inflammation even in the absence of OX40 costimulation. We found that OX40-deficient mice were compromised in generating Th2 cells, airway eosinophilia, and IgE responses. In contrast, OX40-deficient/survivin transgenic mice generated normal Th2 responses and exhibited strong lung inflammation. These results suggest that OX40 costimulation crucially engages survivin during antigen-mediated Th2 responses. These findings also promote the notion that OX40 costimulation regulates allergic responses or lung inflammation by targeting survivin thereby enhancing T-cell proliferation and resulting in more differentiated Th2 cells in the allergic inflammatory response.
Authors:
Fengyang Lei; Jianyong Song; Rizwanul Haque; Xiaofang Xiong; Deyu Fang; Yuzhang Wu; Susanne M A Lens; Michael Croft; Jianxun Song
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2013-05-28
Journal Detail:
Title:  European journal of immunology     Volume:  43     ISSN:  1521-4141     ISO Abbreviation:  Eur. J. Immunol.     Publication Date:  2013 Jul 
Date Detail:
Created Date:  2013-07-05     Completed Date:  2013-09-09     Revised Date:  2014-01-01    
Medline Journal Info:
Nlm Unique ID:  1273201     Medline TA:  Eur J Immunol     Country:  Germany    
Other Details:
Languages:  eng     Pagination:  1914-24     Citation Subset:  IM    
Copyright Information:
© 2013 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cell Differentiation / immunology
Hypersensitivity / immunology*,  metabolism
Inhibitor of Apoptosis Proteins / immunology*,  metabolism
Lymphocyte Activation / immunology
Mice
Mice, Inbred C57BL
Mice, Transgenic
Pneumonia / immunology*,  metabolism
Receptors, OX40 / deficiency,  immunology*
Repressor Proteins / immunology*,  metabolism
Th2 Cells / cytology,  immunology*
Grant Support
ID/Acronym/Agency:
K18 CA151798/CA/NCI NIH HHS; K18CA151798/CA/NCI NIH HHS; R01 AI079056/AI/NIAID NIH HHS; R01AI079056/AI/NIAID NIH HHS
Chemical
Reg. No./Substance:
0/Birc5 protein, mouse; 0/Inhibitor of Apoptosis Proteins; 0/Receptors, OX40; 0/Repressor Proteins; 0/Tnfrsf4 protein, mouse

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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