Inhibition of T cell costimulation abrogates airway hyperresponsiveness in a murine model
Autor: | Yi Wang, David A. Mark, James A. Listman, David C. Christiani, David L. Perkins, Patricia W. Finn, Carolyn E. Donovan, Manuela Cernadas, S J Krinzman, I Katona, K Nassr, Lester Kobzik, G. T. De Sanctis |
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Rok vydání: | 1996 |
Předmět: |
Male
Ovalbumin T-Lymphocytes T cell Biology Immunoglobulin E Major histocompatibility complex Bronchoalveolar Lavage Bronchoconstrictor Agents Mice CD28 Antigens Antigen Hypersensitivity medicine Animals Cytotoxic T cell Receptor Lung Methacholine Chloride Inflammation Mice Inbred BALB C Histocytochemistry Airway Resistance CD28 General Medicine Flow Cytometry medicine.disease Immunohistochemistry respiratory tract diseases Disease Models Animal medicine.anatomical_structure Bronchial hyperresponsiveness Immunoglobulin G Immunology biology.protein Cell Division Research Article |
Zdroj: | Journal of Clinical Investigation. 98:2693-2699 |
ISSN: | 0021-9738 |
DOI: | 10.1172/jci119093 |
Popis: | Activation of naive T cells requires at least two signals. In addition to the well characterized interaction of the T cell antigen receptor with the antigen/MHC expressed on an antigen-presenting cell, T cell activation also requires costimulation by a second set of signals. The best characterized costimulatory receptor is CD28, which binds to a family of B7 ligands expressed on antigen-presenting cells. In asthma, although activated T cells play a role in the initiation and maintenance of airway inflammation, the importance of T cell costimulation in bronchial hyperresponsiveness had not been characterized. Therefore, we tested the hypothesis that inhibition of the CD28:B7 costimulatory pathway would abrogate airway hyperresponsiveness. Our results show that blockade of costimulation with CTLA4-Ig, a fusion protein known to prevent costimulation by blocking CD28:B7 interactions, inhibits airway hyperresponsiveness, inflammatory infiltration, expansion of thoracic lymphocytes, and allergen-specific responsiveness of thoracic T cells in this murine model of allergic asthma. |
Databáze: | OpenAIRE |
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