| First Author | Hamelmann E | Year | 1997 |
| Journal | Proc Natl Acad Sci U S A | Volume | 94 |
| Issue | 4 | Pages | 1350-5 |
| PubMed ID | 9037056 | Mgi Jnum | J:38611 |
| Mgi Id | MGI:85998 | Doi | 10.1073/pnas.94.4.1350 |
| Citation | Hamelmann E, et al. (1997) Allergic airway sensitization induces T cell activation but not airway hyperresponsiveness in B cell-deficient mice. Proc Natl Acad Sci U S A 94(4):1350-5 |
| abstractText | B cells play an important role in the allergic response by producing allergen-specific Igs as well as by serving as antigen-presenting cells. We studied the involvement of B cells in the development of responses in a murine model of allergic airway sensitization. Normal and B cell-deficient (muMt-/-) B10.BR mice were sensitized via the airways to ovalbumin; Ig production, cytokine elaboration from local lymph node cells, development of airway hyperresponsiveness, and histological changes in the airways were evaluated. Both strains of mice had increased production of T helper 2-like cytokines and developed an accumulation of eosinophils in the bronchial tissue after airway sensitization. However, only wild-type mice produced allergen-specific antibodies and exhibited altered airway function. B cell-deficient mice reconstituted with anti-ovalbumin IgE during the course of sensitization developed increases in airway responsiveness. These results indicated that neither B cells nor IgE were necessary for the induction of a T helper 2-type cytokine response or eosinophil infiltration of the airways after allergic sensitization but that IgE was required as a second signal for the development of airway hyperresponsiveness in this model of airway sensitization. |
