Ovalbumin aerosols induce airway hyperreactivity in naive DO11.10 T cell receptor transgenic mice without pulmonary eosinophilia or OVA-specific antibody
Ja. Wilder et al., Ovalbumin aerosols induce airway hyperreactivity in naive DO11.10 T cell receptor transgenic mice without pulmonary eosinophilia or OVA-specific antibody, J LEUK BIOL, 69(4), 2001, pp. 538-547
The pathobiology of allergic asthma is being studied using murine models, m
ost of which use systemic printing followed by pulmonary challenges with th
e immunizing antigen. In general, mice develop eosinophilic pulmonary infla
mmation, increased antigen-specific immunoglobulins, and airway hyperreacti
vity (AHR), all of which are dependent on antigen-specific T cell activatio
n. To establish a model of allergic asthma, which did not require systemic
priming, we exposed DO11.10 T cell receptor transgenic mice, which have an
expanded repertoire of ovalbumin (OVA), peptide-specific T cells, to limite
d aerosols of OVA protein. DO11.10 +/- mice developed AHR in the absence of
increases in total serum IgE, OVA-specific IgG, or eosinophilia, The AHR w
as accompanied by pulmonary recruitment of antigen-specific T cells with de
creased expression of CD62L and CD45RB and increased expression of CD69, a
phenotype indicative of T cell activation. Our results support recent hypot
heses that T cells mediate AHR directly.