The Journal of allergy and clinical immunology · 2025
Mouse TH2 cell extracellular vesicles promote eosinophil survival through the surface cytokine cargo IL-3.
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Bunn Kaitlyn E, Giese-Byrne Brenna G, Blatt Alexander M, Newcomb Dawn C, Pua Heather H
Аннотация
BACKGROUND: Extracellular vesicles (EVs) mediate intercellular communication during immune responses. EVs are abundant in respiratory biofluids, and the composition of EVs in the lung changes during inflammation.
OBJECTIVE: We sought to quantify the contribution of T cells to airway EVs in eosinophilic lung inflammation and ascertain their function during a type 2 inflammatory response.
METHODS: Genetic membrane tagging was combined with single vesicle flow cytometry to quantify T-cell EVs in the airways of mice challenged with ovalbumin or house dust mite. EVs were purified from mouse TH2 cell cultures, and their functions on eosinophils were assessed by flow cytometry and RNA sequencing. TH2 cell EVs were instilled into the lungs of mice to determine effects on lung eosinophilia. Finally, the function of an EV protein cargo was tested using inhibitors and blocking antibodies.
RESULTS: T-cell EVs are increased in the airways of mice after ovalbumin- or house dust mite-induced inflammation. EVs secreted by TH2 cells inhibit apoptosis and induce activating pathways in eosinophils in vitro. This effect depends on restimulation through the T-cell receptor. TH2 cell EVs prolong eosinophilia in vivo during acute eosinophilic inflammation. TH2 cell EVs carry the cytokine IL-3 as a surface cargo, which inhibits apoptosis by activating JAK1/2-dependent pro-survival programs in eosinophils.
CONCLUSIONS: TH2 cell EVs promote eosinophil survival through the EV cargo IL-3, supporting a role for EVs as vehicles of cytokine-based communication in lung inflammation.
OBJECTIVE: We sought to quantify the contribution of T cells to airway EVs in eosinophilic lung inflammation and ascertain their function during a type 2 inflammatory response.
METHODS: Genetic membrane tagging was combined with single vesicle flow cytometry to quantify T-cell EVs in the airways of mice challenged with ovalbumin or house dust mite. EVs were purified from mouse TH2 cell cultures, and their functions on eosinophils were assessed by flow cytometry and RNA sequencing. TH2 cell EVs were instilled into the lungs of mice to determine effects on lung eosinophilia. Finally, the function of an EV protein cargo was tested using inhibitors and blocking antibodies.
RESULTS: T-cell EVs are increased in the airways of mice after ovalbumin- or house dust mite-induced inflammation. EVs secreted by TH2 cells inhibit apoptosis and induce activating pathways in eosinophils in vitro. This effect depends on restimulation through the T-cell receptor. TH2 cell EVs prolong eosinophilia in vivo during acute eosinophilic inflammation. TH2 cell EVs carry the cytokine IL-3 as a surface cargo, which inhibits apoptosis by activating JAK1/2-dependent pro-survival programs in eosinophils.
CONCLUSIONS: TH2 cell EVs promote eosinophil survival through the EV cargo IL-3, supporting a role for EVs as vehicles of cytokine-based communication in lung inflammation.