Details

Autor(en) / Beteiligte

• Xu, Haifeng C.
• Huang, Jun
• Pandyra, Aleksandra A.
• Lang, Elisabeth
• Zhuang, Yuan
• Thöns, Christine
• Timm, Jörg
• Häussinger, Dieter
• Colonna, Marco
• Cantor, Harvey
• Lang, Karl S.
• Lang, Philipp A.

Titel

Lymphocytes Negatively Regulate NK Cell Activity via Qa-1b following Viral Infection

Ist Teil von

• Cell reports (Cambridge), 2017-11, Vol.21 (9), p.2528-2540

Ort / Verlag

United States: Elsevier Inc

Erscheinungsjahr

2017

Link zum Volltext

Quelle

Alma/SFX Local Collection

Beschreibungen/Notizen

• 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. [Display omitted] •Infection induces Qa-1b expression on B and T lymphocytes•Qa-1b promotes anti-viral immunity and prevents chronic viral infection•Qa-1b expression on B lymphocytes inhibits NK cell-mediated regulation of T cells Xu et al. show that Qa-1b expression is predominantly upregulated on B lymphocytes following lymphocytic choriomeningitis virus infection. Absence of Qa-1b results in increased NK cell-mediated regulation of anti-viral T cells, limited anti-viral immunity, and chronic viral infection.