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Войти в исследования Clinical and translational allergy · 2025
ST2+ Erythroid Progenitors Suppress Allergic Asthma by Scavenging IL-33 in Young Mice.
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Li Chang, Liu Jie, Li Xiaoshi, Chen Wenlong, Zhang Ying, Sun Heng, Zheng Cunni, Liu Quan
Аннотация
BACKGROUND: Although IL-33/ST2 signaling has been implicated in adult asthma, its contribution to early-onset allergic asthma remains poorly understood. Here, we examined the postnatal dynamics of IL-33 and its regulation by splenic ST2+ erythroid progenitors (EPs).
METHODS: Plasma IL-33 levels were measured in neonatal and young mice. Wild Type (WT) and Il33-/- mice were exposed to house dust mite (HDM) to assess airway inflammation and asthma. ST2+ EPs were analyzed for IL-33 responsiveness, transcriptomic/epigenomic profiles, and IL-33 scavenging capacity. EP depletion was performed to evaluate their role in HDM-induced inflammation.
RESULTS: Plasma IL-33 levels fluctuated during the postnatal period, peaking at postnatal day 7 (PND7). WT mice exhibited more severe HDM-induced airway inflammation than Il33-/- mice. Splenic ST2+ EPs, abundant in early life but absent by PND28, displayed minimal IL-33-induced signaling or transcriptomic/epigenomic alterations, yet efficiently scavenged IL-33. Depletion of EPs exacerbated HDM-induced inflammation, accompanied by increased T follicular helper cells (Tfh) and IgE+ B cells.
CONCLUSION: ST2+ EPs function as transient IL-33 scavengers during early life, attenuating its pro-asthmatic effects and preserving immune homeostasis.
METHODS: Plasma IL-33 levels were measured in neonatal and young mice. Wild Type (WT) and Il33-/- mice were exposed to house dust mite (HDM) to assess airway inflammation and asthma. ST2+ EPs were analyzed for IL-33 responsiveness, transcriptomic/epigenomic profiles, and IL-33 scavenging capacity. EP depletion was performed to evaluate their role in HDM-induced inflammation.
RESULTS: Plasma IL-33 levels fluctuated during the postnatal period, peaking at postnatal day 7 (PND7). WT mice exhibited more severe HDM-induced airway inflammation than Il33-/- mice. Splenic ST2+ EPs, abundant in early life but absent by PND28, displayed minimal IL-33-induced signaling or transcriptomic/epigenomic alterations, yet efficiently scavenged IL-33. Depletion of EPs exacerbated HDM-induced inflammation, accompanied by increased T follicular helper cells (Tfh) and IgE+ B cells.
CONCLUSION: ST2+ EPs function as transient IL-33 scavengers during early life, attenuating its pro-asthmatic effects and preserving immune homeostasis.