Generation of cellular immune memory and B-cell immunity is impaired by natural killer cells

Carolyn Rydyznski, Keith A. Daniels, Erik P. Karmele, Taylor R. Brooks, Sarah E. Mahl, Michael T. Moran, Caimei Li, Rujapak Sutiwisesak, Raymond M. Welsh and Stephen N. Waggoner ()
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Carolyn Rydyznski: Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center
Keith A. Daniels: University of Massachusetts Medical School
Erik P. Karmele: Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center
Taylor R. Brooks: Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center
Sarah E. Mahl: Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center
Michael T. Moran: Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center
Caimei Li: Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center
Rujapak Sutiwisesak: Program in Immunology and Microbiology, University of Massachusetts Medical School
Raymond M. Welsh: University of Massachusetts Medical School
Stephen N. Waggoner: Center for Autoimmune Genomics and Etiology, Cincinnati Children’s Hospital Medical Center

Nature Communications, 2015, vol. 6, issue 1, 1-14

Abstract: Abstract The goal of most vaccines is the induction of long-lived memory T and B cells capable of protecting the host from infection by cytotoxic mechanisms, cytokines and high-affinity antibodies. However, efforts to develop vaccines against major human pathogens such as HIV and HCV have not been successful, thereby highlighting the need for novel approaches to circumvent immunoregulatory mechanisms that limit the induction of protective immunity. Here, we show that mouse natural killer (NK) cells inhibit generation of long-lived virus-specific memory T- and B cells as well as virus-specific antibody production after acute infection. Mechanistically, NK cells suppressed CD4 T cells and follicular helper T cells (TFH) in a perforin-dependent manner during the first few days of infection, resulting in a weaker germinal centre (GC) response and diminished immune memory. We anticipate that innovative strategies to relieve NK cell-mediated suppression of immunity should facilitate development of efficacious new vaccines targeting difficult-to-prevent infections.

Date: 2015
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DOI: 10.1038/ncomms7375

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