V-beta-8+ T lymphocytes are essential in the regulation of airway hyperresponsiveness and bronchial eosinophilia but not in allergen-specific IgE in a murine model of allergic asthma

Background There is increasing evidence that in allergic asthma the inflammatory process is regulated by T lymphocytes. In BALB/c mice the majority of ovalbumin responsive T lymphocytes express the V8.1 and V8.2 T-cell receptor. Objective We analysed the contribution of V8 T lymphocytes during the sensitization and challenge phase in the regulation of antigen-specific IgE, airway hyperresponsiveness and cellular infiltration in the airways in a murine model of allergic asthma. Methods Mice strains genetically lacking (SJL/J and SJA/9) and expressing (BALB/c) the V8 T cell receptor were used. In addition, prior to the sensitization and prior to the challenge BALB/c mice were treated with antibodies to V8. Mice were sensitized with ovalbumin, followed by repeated challenge with ovalbumin or saline aerosols. Results In ovalbumin challenged BALB/c mice treated with control antibody a significant increase in eosinophils in the bronchoalveolar lavage, airway hyperresponsiveness and increased serum levels of ovalbumin-specific IgE were observed compared to control mice. Treatment of BALB/c mice with antibodies to V8 prior to the sensitization or prior to the challenge period completely inhibited the ovalbumin induced infiltration of eosinophils and airway hyperresponsiveness, while ovalbumin-specific IgE was slightly decreased. In SJA/9 and SJL/J mice ovalbumin challenge did not induce eosinophilic infiltration and airway hyperresponsiveness. In SJL/J mice ovalbumin challenge induced an upregulation of ovalbumin-specific IgE, however, in SJA/9 mice no upregulation was observed. Conclusion It is demonstrated that V8 T lymphocytes are essential for infiltration of eosinophils in the airways and development of airway hyperresponsiveness in a murine model of allergic asthma. In contrast, although V8 T lymphocytes seem to be important for the extent of IgE levels, no essential role for V8 T lymphocytes in the induction of antigen-specific IgE was observed