Journal
AUTOIMMUNITY
Volume 40, Issue 7, Pages 483-488Publisher
TAYLOR & FRANCIS LTD
DOI: 10.1080/08916930701651139
Keywords
DRAK2; virus; T cells; memory; host-defense
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Funding
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI063419] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS041249] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI063419] Funding Source: Medline
- NINDS NIH HHS [NS41249] Funding Source: Medline
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The contribution of DRAK2 [death-associated protein kinase (DAPK)-related apoptosis-inducing kinase 2] to anti-viral memory T cell responses following infection with mouse hepatitis virus (MHV) was examined. DRAK2 is a lymphoid-enriched serine/threonine kinase that is an important regulatory molecule involved in modulating T cell responses. Memory T cells derived from MHV-immunized Drak2(-/-) mice exhibited amplified proliferation and IFN-gamma secretion following stimulation with viral epitopes. Transfer of Drak2(-/-) memory T cells into Rag1(-/-) mice infected intracerebrally with MHV resulted in accelerated clearance of virus from the brain. Thus, DRAK2 may be a novel target for stimulating protective immunity to viral pathogens.
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