Drak2 is not required for tumor surveillance and suppression
| Autor: | Tarsha L. Harris, Md. Hasan Zaki, Benjamin A. Edwards, Thirumala-Devi Kanneganti, Jack D. Bui, Helen Floersh, Maureen A. McGargill, John R. Lukens, Peter Vogel |
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| Rok vydání: | 2015 |
| Předmět: |
Graft Rejection
Male medicine.medical_specialty Multiple Sclerosis Short Communication medicine.medical_treatment Immunology Apoptosis Protein Serine-Threonine Kinases medicine.disease_cause Organ transplantation law.invention Autoimmunity Mice Immune system law Cell Line Tumor Animals Humans Immunology and Allergy Medicine Immunologic Surveillance Immunosuppression Therapy Mice Knockout Autoimmune disease business.industry Tumor Suppressor Proteins Multiple sclerosis Sarcoma Immunosuppression Organ Transplantation General Medicine medicine.disease Mice Inbred C57BL Disease Models Animal Diabetes Mellitus Type 1 Suppressor business |
| Zdroj: | International Immunology. 27:161-166 |
| ISSN: | 1460-2377 0953-8178 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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