| Literature DB >> 25568303 |
Benjamin A Edwards1, Tarsha L Harris1, Helen Floersh1, John R Lukens1, Md Hasan Zaki1, Peter Vogel2, Thirumala-Devi Kanneganti1, Jack D Bui3, Maureen A McGargill4.
Abstract
Drak2 is a promising therapeutic target to treat organ-specific autoimmune diseases such as type 1 diabetes and multiple sclerosis without causing generalized immune suppression. Inhibition of Drak2 may also prevent graft rejection following organ transplantation. However, Drak2 may function as a critical tumor suppressor, which would challenge the prospect of targeting Drak2 for therapeutic treatment. Thus, we examined the susceptibility of Drak2 (-/-) mice in several tumor models. We show that Drak2 is not required to prevent tumor formation in a variety of settings. Therefore, Drak2 does not function as an essential tumor suppressor in in vivo tumor models. These data further validate Drak2 as a viable therapeutic target to treat autoimmune disease and graft rejection. Importantly, these data also indicate that while Drak2 may induce apoptosis when overexpressed in cell lines, it is not an essential tumor suppressor. © The Japanese Society for Immunology. 2015. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.Entities:
Keywords: autoimmunity; regulation of immune responses; tumor surveillance
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Year: 2015 PMID: 25568303 PMCID: PMC4817074 DOI: 10.1093/intimm/dxu146
Source DB: PubMed Journal: Int Immunol ISSN: 0953-8178 Impact factor: 4.823