Journal
CELL REPORTS
Volume 21, Issue 9, Pages 2528-2540Publisher
CELL PRESS
DOI: 10.1016/j.celrep.2017.11.001
Keywords
-
Categories
Funding
- Alexander von Humboldt Foundation [SKA2010]
- German Research Council [SFB974, LA2558/3-1, LA2558/5-1, RTG1949]
- Jurgen Manchot Graduate School (MOI III)
- NIH [AI037562]
- NIH
Ask authors/readers for more resources
NK cells can reduce anti-viral T cell immunity during chronic viral infections, including infection with the lymphocytic choriomeningitis virus (LCMV). However, regulating factors that maintain the equilibrium between productive T cell and NK cell immunity are poorly understood. Here, we show that a large viral load resulted in inhibition of NK cell activation, which correlated with increased expression of Qa-1b, a ligand for inhibitory NK cell receptors. Qa-1b was predominantly upregulated on B cells following LCMV infection, and this upregulation was dependent on type I interferons. Absence of Qa-1b resulted in increased NK cell-mediated regulation of anti-viral T cells following viral infection. Consequently, anti-viral T cell immunity was reduced in Qa-1b-and NKG2A-deficient mice, resulting in increased viral replication and immunopathology. NK cell depletion restored anti-viral immunity and virus control in the absence of Qa-1b. Taken together, our findings indicate that lymphocytes limit NK cell activity during viral infection in order to promote anti-viral T cell immunity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available