Development of Spontaneous Airway Changes Consistent with Human Asthma in Mice Lacking T-bet-Reference-Cited by-同舟云学术

Development of Spontaneous Airway Changes Consistent with Human Asthma in Mice Lacking T-bet

Published:2002-01-11 Issue:5553 Volume:295 Page:336-338
ISSN:0036-8075
Container-title:Science
language:en
Short-container-title:Science

Author:

Finotto Susetta¹,Neurath Markus F.²,Glickman Jonathan N.³,Qin Shixin⁴,Lehr Hans A.⁵,Green Francis H. Y.⁶,Ackerman Kate¹,Haley Kathleen¹,Galle Peter R.⁷,Szabo Susanne J.⁸,Drazen Jeffrey M.¹⁸,De Sanctis George T.¹,Glimcher Laurie H.⁸

Affiliation:

1. Critical Care and Pulmonary Division,

2. Division of Gastroenterology,

3. Department of Pathology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.

4. Millenium Pharmaceuticals, Cambridge, MA 02138, USA.

5. Department of Pathology, University of Mainz, Mainz 55131, Germany.

6. Department of Pathology and Laboratory Medicine University of Calgary, Alberta, Canada T2N 4N1.

7. Medical Clinic I, University of Mainz, Mainz 55131, Germany.

8. Harvard School of Public Health and Harvard Medical School, Harvard Medical School, Boston, MA 02115, USA.

Abstract

Human asthma is associated with airway infiltration by T helper 2 (T H 2) lymphocytes. We observed reduced expression of the T H 1 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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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