Rapid loss of group 1 innate lymphoid cells during blood stage Plasmodium infection (48968)
Innate lymphoid cells (ILCs) resemble T helper (Th) cells in terms of transcription factor requirements and cytokine expression profiles, but do not express antigen-specific receptors. Group 1 ILCs consist of natural killer (NK) cells and type 1 ILCs (ILC1s). Together, they share many characteristics with Th1 cells such as a requirement for the transcription factor T-bet and the ability to produce IFNγ. However, the developmental relationship between NK cells and ILC1s is still a matter of debate. An ILC1 subset that is liver-resident has recently been described. Given the resemblance between ILC1s and Th1 cells, and the importance of Th1 cells in the anti-parasitic immune response, we aimed to characterise the role of ILCs during Plasmodium infection. Initial findings suggested that ILC1s and NK cells have a limited role in conferring protection or causing pathology during P. chabaudi chabaudi AS (PcAS) infection. However, in a controlled human malaria infection study, we showed that the frequencies of circulating ILC1s and NKs were decreased at the peak of infection, compared to frequencies before infection. A similar observation was made for liver and splenic ILC1s in PcAS-infected mice. The decrease in liver ILC1 frequencies in mice was associated with increased apoptosis but did not directly relate to peripheral blood parasitemia. Together, our results show that ILC1s are lost early during rodent and human malaria parasite infection, and this observation may explain the limited role for ILC1s and NK cells in controlling blood stage malaria.