Journal
NATURE COMMUNICATIONS
Volume 9, Issue -, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41467-018-06978-5
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Funding
- BeIPD ULiege-Marie Curie COFUND fellowship
- NIAID Schistosomiasis Resource Center of the Biomedical Research Institute (Rockville, MD) through NIH-NIAID [HHSN272201000005I]
- Wellcome Trust investigator award [106122]
- Wellcome Trust [104111]
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Infection with parasitic helminths can imprint the immune system to modulate bystander inflammatory processes. Bystander or virtual memory CD8(+) T cells (T-vm) are nonconventional 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-vm compartment. Here, we show that helminths expand CD44(hi)CD62L(hi)CXCR3(hi)CD49d(lo) T-vm cells through direct IL-4 signaling in CD8(+) T cells. Importantly, helminth-mediated conditioning of T-vm 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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