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
Article first published online: 25 DEC 2001
Blackwell Science Ltd, Oxford
Clinical & Experimental Allergy
Volume 28, Issue 12, pages 1571–1580, December 1998
How to Cite
Hofstra, Van Ark, Savelkoul, Cruikshank, Nijkamp and Van Oosterhout (1998), 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. Clinical & Experimental Allergy, 28: 1571–1580. doi: 10.1046/j.1365-2222.1998.00387.x
- Issue published online: 25 DEC 2001
- Article first published online: 25 DEC 2001
- T lymphocytes;
- airway hyperresponsiveness
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.
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.
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.
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.
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.