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Non-redundant roles for ILC2 and TH2 cells during anamnestic lung Type 2 immunity

ABSTRACT: Type 2 immune responses help with wound healing and clearing helminth infections, but the distinct roles of group 2 innate lymphoid cells (ILC2s) and T-helper 2 (TH2) cells are not fully understood. In this study, we examined whether ILC2s and TH2 cells are necessary or sufficient to repair lung injury and prevent re-infection with the parasite Nippostrongylus brasiliensis. Surprisingly, removing TH2 cells before re-infection did not affect lung healing or worm clearance. However, mice lacking ILC2s (LCR1-/-) showed severe IL-17-related lung bleeding and poor parasite clearance. Activated ILC2s expressed high levels of Amphiregulin (Areg) and Tph1, and Areg+ ILC2s were more abundant than TH2 cells in re-infected lungs. Although treatment with recombinant Areg increased TH2 cell numbers and improved worm clearance, it did not reduce lung injury in ILC2-deficient mice. Interestingly, serotonin levels influenced IL-17-driven lung damage regardless of parasite burden. Our findings suggest that while TH2 cells help fight infection, ILC2s play a unique and essential role in repairing lung tissue.

ORGANISM(S): Mus musculus

PROVIDER: GSE295590 | GEO | 2026/04/01

REPOSITORIES: GEO

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Project description:Armigeres subalbatus is a natural vector of the filarial worm Brugia pahangi, but it kills Brugia malayi microfilariae (mf) by melanotic encapsulation. Because B. malayi and B. pahangi are morphologically and biologically similar, this mosquito-parasite system serves as a valuable model for studying resistance mechanisms in mosquito vectors. Comparing Ar. subalbatus-B. pahangi susceptibility and Ar. subalbatus-B. malayi refractoriness could provide significant insight into recognition mechanisms required to mount an effective anti-filarial worm immune response in the mosquito, as well as provide considerable detail into the molecular components involved in vector competence. Accordingly, we initiated transcriptome profiling studies of Ar. subalbatus in relation to filarial worm infection to provide information on the molecular components involved in B. pahangi susceptibility for comparison with our earlier studies on B. malayi refractoriness (Aliota et al., 2007). In addition, these studies also provide information on the infection response of a natural vector, i.e., the overall transcriptional and physiological change that occurs in the mosquito as a result of parasite infection, for comparison with our previous studies that employed a highly susceptible laboratory model, Aedes aegypti (Erickson et al., 2009). The time course chosen facilitated an examination of key events in the development of the parasite, beginning with the very start of filarial worm infection and spanning to well after infective-stage parasites had completed development in the mosquito. Herein, we demonstrate that filarial worm susceptibility in Ar. subalbatus is a highly complex process during the first 24 hours of infection. It is a process that involves many factors of both known and unknown function which are most likely associated with filarial worm penetration through the midgut lumen, invasion into thoracic muscle cells, and maintenance of homeostasis in the hemolymph environment. The data show that there are distinct and separate transcriptional patterns associated with filarial worm susceptibility as compared to refractoriness, and that an infection response in Ar. subalbatus, a natural vector, can differ significantly from that observed in Ae. aegypti, a common laboratory model. Finally, the data presented herein provide us with a cadre of information to design wet lab experiments and select candidates for further study to more fully dissect the nature of the anti-filarial worm immune response in this mosquito-parasite system.

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Non-redundant roles for ILC2 and TH2 cells during anamnestic lung Type 2 immunity

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