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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Role of CD4-positive T cells in the pathogenesis of nasal allergy in the murine model.

BACKGROUND: Antigen-induced upregulation of cytokines, especially Th2-type cytokines, has been proven to be closely related to allergic inflammation in nasal allergy. CD4-positive T cells are supposed to play an important role not only in the induction of allergy but also in allergic inflammation. METHODS: The anti-CD4 mAb was administered to the murine model of nasal allergy either at the beginning of sensitization, just before antigen challenge or during a topical booster sensitization. Then, the effects on the antigen-induced nasal responses and the serum level of antigen-specific IgE antibody were evaluated. RESULTS: When the mAb was applied at the beginning of sensitization, the early-phase nasal symptoms and the late-phase nasal eosinophilia were significantly inhibited, and the 8-day passive cutaneous anaphylaxis ( PCA) titer tended to be inhibited. When the mAb was applied just before the challenge, there were no differences in the nasal symptoms, the nasal eosinophilia or the 8-day PCA titer between the mAb-treated animals and the control animals. When the mAb was applied during a topical booster sensitization, the nasal eosinophilia, the 8-day PCA titer and histamine hypersensitivity were significantly suppressed in the treated animals. CONCLUSION: CD4-positive T cells play an important role in the induction of IgE-mediated nasal allergy, occurrence of late-phase allergic inflammation and histamine hypersensitivity, but not in antigen-induced early-phase nasal symptoms in the murine model. In cases of chronic topical antigen exposure, however, the suppressive effects of a single application of the anti-CD4 mAb are not remarkable.[1]

References

  1. Role of CD4-positive T cells in the pathogenesis of nasal allergy in the murine model. Ogasawara, H., Asakura, K., Saito, H., Kataura, A. Int. Arch. Allergy Immunol. (1999) [Pubmed]
 
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