6533b86efe1ef96bd12cbf3d
RESEARCH PRODUCT
Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet.
Shixin QinJonathan N. GlickmanSusetta FinottoSusanne J. SzaboMarkus F. NeurathKathleen J. HaleyKate G. AckermanLaurie H. GlimcherGeorge T. De SanctisJeffrey M. DrazenPeter R. GalleHans A. LehrFrancis H. Y. Greensubject
TBX21CD4-Positive T-LymphocytesAdoptive cell transferRatónchemical and pharmacologic phenomenaMice SCIDMicemedicineAnimalsHumansLungAsthmaMice KnockoutMultidisciplinarybusiness.industryRespiratory diseaseGene targetinghemic and immune systemsT lymphocyteAllergensmedicine.diseaseAdoptive TransferAsthmarespiratory tract diseasesDisease Models AnimalCollagen Type IIIKnockout mouseImmunologyGene TargetingCytokinesInterleukin-4Bronchial HyperreactivityInterleukin-5businessT-Box Domain ProteinsBronchoalveolar Lavage FluidTranscription Factorsdescription
Human asthma is associated with airway infiltration by T helper 2 (TH2) lymphocytes. We observed reduced expression of the TH1 transcription factor, T-bet, in T cells from airways of patients with asthma compared with that in T cells from airways of nonasthmatic patients, suggesting that loss of T-bet might be associated with asthma. Mice with a targeted deletion of the T-bet gene and severe combined immunodeficient mice receiving CD4+cells from T-bet knockout mice spontaneously demonstrated multiple physiological and inflammatory features characteristic of asthma. Thus, T-bet deficiency, in the absence of allergen exposure, induces a murine phenotype reminiscent of both acute and chronic human asthma.
| year | journal | country | edition | language |
|---|---|---|---|---|
| 2002-01-12 | Science (New York, N.Y.) |