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Vβ8+ T lymphocytes are essential in the regulation of airway hyperresponsiveness and bronchoalveolar eosinophilia but not in allergen-specific IgE in a murine model of allergic asthma

Authors


Hofstra Department of Pharmacology and Pathophysiology, Utrecht University, P.O. Box 80.082, 3508 TB Utrecht, The Netherlands.

Abstract

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 Vβ8.1+ and Vβ8.2+ T-cell receptor.

Objective

We analysed the contribution of Vβ8+ 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 Vβ8+ T cell receptor were used. In addition, prior to the sensitization and prior to the challenge BALB/c mice were treated with antibodies to Vβ8. 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 Vβ8 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 Vβ8+ 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 Vβ8+ T lymphocytes seem to be important for the extent of IgE levels, no essential role for Vβ8+ T lymphocytes in the induction of antigen-specific IgE was observed.

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