RESUMO
@#【Objectives】Todevelopagroup2innatelymphoidcell（ILC2）-dominantallergicairwayinflammation modelinwildtypeC57BL/6andT/Bcell-deficientRag1-/- mice.【Methods】FemaleC57BL/6andRag1-/- micewere randomlydividedintocontrolandmodelgroups.Themiceinmodelgroupswereadministeredintratracheallywith1μg IL-33in20μLH2Oondays1，3and5，andthecontrolmicewereadministeredaccordinglywith20μLH2O.Onday6， themiceweresacrificedforcollectionofbronchoalveolarlavagefluid（BALF）andthelungs.Thepulmonaryinflammation inmicewasevaluatedbypathologicalstainingforlungtissues，ELISAforlevelsofcytokinesinBALF，andflowcytometry analyses of ILC2 and inflammatory cells.【Results】Both the C57BL/6 and Rag1-/- mice with the treatment of IL-33 exhibitedobviouseosinophilicairwayinflammationinperi-trachealarea（P<0.05）andgobletcellhyperplasiainairway epithelium（P<0.05）.Comparedwiththecontrolmice，numbersofeosinophils（P<0.05）andneutrophils（P<0.05） aswellaslevelsofIL-5（P <0.05）andIL-13（P <0.05）inBALFwereincreasedinthemodelgroup.Inaddition， significantlyhigher levels of ILC2 were found in lung tissues of the model mice.【Conclusion】The ILC2-dominant allergicairwayinflammationwassuccessfullydevelopedinbothC57BL/6andRag1-/-mice，whichprovidedtheapproach toinvestigatetheroleofILC2inasthmaandallergicrhinitis.
