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Helminth-induced IL-4 expands bystander memory CD8 T cells for early control of viral infection
Rolot, M Dougall, A.M Chetty, A Javaux, J Chen, T Xiao, X Machiels, B Selkirk, M.E Maizels, R.M Hokke, C
Rolot, M
Dougall, A.M
Chetty, A
Javaux, J
Chen, T
Xiao, X
Machiels, B
Selkirk, M.E
Maizels, R.M
Hokke, C
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Abstract
Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8 T cells (T) 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 T compartment. Here, we show that helminths expand CD44CD62LCXCR3CD49d T cells through direct IL-4 signaling in CD8 T cells. Importantly, helminth-mediated conditioning of T 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.
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2018-10-30
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Nature Communications
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Rolot M, Dougall AM, Chetty A, Javaux J, Chen T, Xiao X, Machiels B, Selkirk ME, Maizels RM, Hokke C, Denis O, Brombacher F, Vanderplasschen A, Gillet L, Horsnell WGC, Dewals BG. Helminth-induced IL-4 expands bystander memory CD8+ T cells for early control of viral infection. Nat Commun. 2018 Oct 30;9(1):4516. doi: 10.1038/s41467-018-06978-5.