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J. Exp. Med.,
Volume 188, Number 9, November 2, 1998 1739-1750
B in the Induction
of Eosinophilia in Allergic Airway Inflammation
By
From the * Department of Internal Medicine, Pulmonary and Critical Care Section, the The molecular mechanisms that contribute to an eosinophil-rich airway inflammation in
asthma are unclear. A predominantly T helper 2 (Th2)-type cell response has been documented
in allergic asthma. Here we show that mice deficient in the p50 subunit of nuclear factor (NF)-
Section of
Immunobiology, and the § Department of Pathology, Yale University School of Medicine, New Haven,
Connecticut 06520
B are incapable of mounting eosinophilic airway inflammation compared with wild-type
mice. This deficiency was not due to a block in T cell priming or proliferation in the p50
/
mice, nor was it due to a defect in the expression of the cell adhesion molecules VCAM-1 and
ICAM-1 that are required for the extravasation of eosinophils into the airways. The major defects in the p50/ mice were the lack of production of the Th2 cytokine interleukin 5 and the
chemokine eotaxin, which are crucial for proliferation and for differentiation and recruitment,
respectively, of eosinophils into the asthmatic airway. Additionally, the p50/ mice were deficient in the production of the chemokines macrophage inflammatory protein (MIP)-1
and
MIP-1
that have been implicated in T cell recruitment to sites of inflammation. These results demonstrate a crucial role for NF-B in vivo in the expression of important molecules that
have been implicated in the pathogenesis of asthma.
B;
interleukin 5;
eotaxin
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