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- W2911528074 abstract "Innate type 2 lymphoid cells (ILC2s) recruit and accumulate in the lung in response to type 2 inflammation. This coincides with production of IL-5 and IL-13 from ILC2s and pulmonary eosinophilia. Although ILC2s have been shown to modulate eosinophil activities, the role of eosinophils in regulating ILC2 responses is less well defined and may represent a novel regulatory feedback pathway. Type 2 pulmonary inflammation was induced by either intratracheal cytokine administration (e.g., IL-33) or using models of ovalbumin or house dust mite allergen sensitization/challenge. Eosinophils were specifically depleted immediately prior to instillation or challenge using inducible eosinophil-deficient mice (iPHIL) mice to determine the role of eosinophils on pulmonary ILC2s in these type 2 inflammation models. Lung-derived ILC2s were cultured with eosinophils to define ILC2 and eosinophil interactions. Activation and chemotaxis of ILC2s were assessed in vitro. Depletion of eosinophils in all type 2 models of respiratory inflammation resulted in a significant reduction of total and activated pulmonary ILC2s. For example, lung IL-13+ILC2s were significantly reduced in IL-33 treated eosinophil-depleted iPHIL mice (236,018± 42,307 vs 106,220 ±26,617 IL-13+ILC2s (p<0.05)). Baseline and saline treated animals had comparable pulmonary ILC2 numbers (<20,000 ILC2s (p>0.05) between eosinophil-proficient and deficient mice. In vitro IL-33 activated eosinophils released chemotactic factors for ILC2s and induced activation of ILC2s through cell-cell contact. Our data demonstrates an underappreciated and significant role for eosinophils in recruitment and activation of ILC2s. These data suggest a reciprocal role for eosinophil-ILC2 interactions in amplification of the type 2 pulmonary inflammatory response." @default.
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- W2911528074 date "2019-02-01" @default.
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- W2911528074 title "Eosinophils Induce Recruitment and Activation of ILC2s" @default.
- W2911528074 doi "https://doi.org/10.1016/j.jaci.2018.12.885" @default.
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