V beta 8(+) T lymphocytes are essential in the regulation of airway hyperresponsiveness and bronchoalveolar eosinophilia but not in allergen-specificIgE in a murine model of allergic asthma

Background There is increasing evidence that in allergic asthma the inflamm atory process is regulated by T lymphocytes. In BALB/c mice the majority of ovalbumin responsive T lymphocytes express the V beta 8.1(+) and V beta 8. 2(+) T-cell receptor. Objective We analysed the contribution of V beta 8(+) T lymphocytes during the sensitization and challenge phase in the regulati on of antigen-specific IgE, airway hyperresponsiveness and cellular infiltr ation 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 V beta 8(+) T cell receptor were used. In addition, prior to th e sensitization and prior to the challenge BALB/c mice were treated with an tibodies to V beta 8. Mice were sensitized with ovalbumin, followed by repe ated 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 we re observed compared to control mice. Treatment of BALB/c mice with antibod ies to V beta 8 prior to the sensitization or prior to the challenge period completely inhibited the ovalbumin induced infiltration of eosinophils and airway hyperresponsiveness, while ovalbumin-specific IEE was slightly decr eased. In SJA/9 and SJL/J mice ovalbumin challenge did not induce eosinophi lic infiltration and airway hyperresponsiveness. In SJL/J mice ovalbumin ch allenge induced an upregulation of ovalbumin-specific IgE, however, in SJA/ 9 mice no upregulation was observed. Conclusion It is demonstrated that V beta 8(+) T lymphocytes are essential for infiltration of eosinophils in the airways and development of airway hy perresponsiveness in a murine model of allergic asthma. In contrast, althou gh V beta 8(+) T lymphocytes seem to be important for the extent of IgE lev els, no essential role for V beta 8(+) T lymphocytes in the induction of an tigen-specific IgE was observed.