Helminth-induced IL-4 expands bystander memory CD8+ T cells for early control of viral infection

Marion Rolot, Annette M. Dougall, Alisha Chetty, Justine Javaux, Ting Chen, Xue Xiao, Bénédicte Machiels, Murray E. Selkirk, Rick M. Maizels, Cornelis Hokke, Olivier Denis, Frank Brombacher, Alain Vanderplasschen, Laurent Gillet, William G. C. Horsnell and Benjamin G. Dewals ()
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Marion Rolot: University of Liège
Annette M. Dougall: University of Liège
Alisha Chetty: University of Cape Town
Justine Javaux: University of Liège
Ting Chen: University of Liège
Xue Xiao: University of Liège
Bénédicte Machiels: University of Liège
Murray E. Selkirk: Imperial College London
Rick M. Maizels: University of Glasgow
Cornelis Hokke: Leiden University Medical Center
Olivier Denis: Communicable and Infectious Diseases
Frank Brombacher: University of Cape Town
Alain Vanderplasschen: University of Liège
Laurent Gillet: University of Liège
William G. C. Horsnell: University of Cape Town
Benjamin G. Dewals: University of Liège

Nature Communications, 2018, vol. 9, issue 1, 1-16

Abstract: Abstract Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8+ T cells (TVM) are non-conventional T cells displaying memory properties that can be generated through responsiveness to interleukin (IL)-4. However, it is not clear if helminth-induced type 2 immunity functionally affects the TVM compartment. Here, we show that helminths expand CD44hiCD62LhiCXCR3hiCD49dlo TVM cells through direct IL-4 signaling in CD8+ T cells. Importantly, helminth-mediated conditioning of TVM cells provided enhanced control of acute respiratory infection with the murid gammaherpesvirus 4 (MuHV-4). This enhanced control of MuHV-4 infection could further be explained by an increase in antigen-specific CD8+ T cell effector responses in the lung and was directly dependent on IL-4 signaling. These results demonstrate that IL-4 during helminth infection can non-specifically condition CD8+ T cells, leading to a subsequently raised antigen-specific CD8+ T cell activation that enhances control of viral infection.

Date: 2018
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DOI: 10.1038/s41467-018-06978-5

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