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Keywords:

  • airway hyper-responsiveness;
  • allergy;
  • asthma;
  • co-stimulation;
  • eosinophilia;
  • immunoglobulin E;
  • T lymphocytes

Summary

Background The existence of a third B7-1/B7-2 receptor was postulated in a recent study using a novel mouse strain lacking both CD28 and CTLA4 (CD28/CTLA4−/−).

Objective In the present study, it was investigated if T cell co-stimulation via the putative B7-1/B7-2 receptor plays a role in the induction of Th2-mediated asthma manifestations in mice.

Methods BALB/c wild-type, CD28/CTLA4−/− and B7-1/B7-2−/− mice were sensitized and aerosol challenged with ovalbumin (OVA).

Results At 24 h after the last aerosol, wild-type mice showed airway hyper-responsiveness in vivo and up-regulated levels of serum OVA-specific IgE compared with the situation shortly before OVA challenge. In addition, eosinophil numbers and IL-5 levels in the broncho-alveolar lavage fluid and Th2 cytokine production by lung cells upon OVA re-stimulation in vitro were observed. In agreement with an earlier study, we failed to induce any of the asthma manifestations in B7-1/B7-2−/− mice. Importantly, also CD28/CTLA4−/− mice showed no asthma manifestations upon OVA sensitization and challenge.

Conclusion These data clearly demonstrate that T cell co-stimulation via the putative B7-1/B7-2 receptor appears to have no role in the induction of Th2-mediated asthma manifestations in this murine model and, conversely, that CD28 signalling is crucial.