E. Hamelmann et al., ALLERGIC AIRWAY SENSITIZATION INDUCES T-CELL ACTIVATION BUT NOT AIRWAY HYPERRESPONSIVENESS IN B-CELL-DEFICIENT MICE, Proceedings of the National Academy of Sciences of the United Statesof America, 94(4), 1997, pp. 1350-1355
B cells play an important role in the allergic response by producing a
llergen-specific Igs as well as by serving as antigen-presenting cells
. We studied the involvement of B cells in the development of response
s in a murine model of allergic airway sensitization, Normal and B cel
l-deficient (mu Mt(-/-)) B10.BR mice were sensitized via the airways t
o ovalbumin; Ig production, cytokine elaboration from local lymph node
cells, development of airway hyperresponsiveness, and histological ch
anges in the airways were evaluated. Both strains of mice had increase
d production of T helper 2-like cytokines and developed an accumulatio
n of eosinophils in the bronchial tissue after airway sensitization. H
owever, 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 neith
er B cells nor IgE were necessary for the induction of a T helper 2-ty
pe cytokine response or eosinophil infiltration of the airways after a
llergic sensitization but that IgE was required as a second signal for
the development of airway hyperresponsiveness in this model of airway
sensitization.