Article: article from journal or magazin.
Development of spontaneous airway changes consistent with human asthma in mice lacking T-bet.
Science (new York, N.y.)
Publication types: Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.Publication Status: ppublish
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.
Adoptive Transfer, Allergens/immunology, Animals, Asthma/immunology, Asthma/metabolism, Bronchial Hyperreactivity/immunology, Bronchial Hyperreactivity/metabolism, Bronchoalveolar Lavage Fluid/immunology, CD4-Positive T-Lymphocytes/immunology, CD4-Positive T-Lymphocytes/transplantation, Collagen Type III/metabolism, Cytokines/metabolism, Disease Models, Animal, Gene Targeting, Humans, Interleukin-4/metabolism, Interleukin-5/metabolism, Lung/immunology, Lung/metabolism, Mice, Mice, Knockout, Mice, SCID, T-Box Domain Proteins, Transcription Factors/deficiency, Transcription Factors/genetics
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