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* DNAX Research Institute of Molecular and Cellular Biology, Palo Alto, CA 94304; and
Schering-Plough Research Institute, Kenilworth, NJ 07033
We have biologically characterized two new members of the IL-17
cytokine family: IL-17F and IL-25. In contrast to conventional in vitro
screening approaches, we have characterized the activity of these new
molecules by direct in vivo analysis and have compared their function
to that of other IL-17 family members. Intranasal administration of
adenovirus expressing IL-17, IL-17C, or IL-17F resulted in
bronchoalveolar lavage neutrophilia and inflammatory gene
expression in the lung. In contrast, intranasal administration of
IL-25-expressing adenovirus or IL-25 protein resulted in the production
of IL-4, IL-5, IL-13, and eotaxin mRNA in the lung and marked
eosinophilia in the bronchoalveolar lavage and lung tissue. Mice given
intranasal IL-25 also developed epithelial cell hyperplasia, increased
mucus secretion, and airway hyperreactivity. IL-25 gene expression was
detected following Aspergillus and
Nippostrongylus infection in the lung and gut,
respectively. IL-25-induced eosinophilia required IL-5 and IL-13, but
not IL-4 or T cells. Following IL-25 administration, the
IL-5+ staining cells were CD45R/B220+,
Thy-1+/-, but were NK1.1-, Ly-6G(GR-1)-, CD4-, CD3-, and
c-kit-negative. 
-common knockout mice did not
develop eosinophilia in response to IL-25, nor were IL-5+
cells detected. These findings suggest the existence of a previously
unrecognized cell population that may initiate Th2-like responses by
responding to IL-25 in vivo. Further, these data demonstrate the
heterogeneity of function within the IL-17 cytokine family and suggest
that IL-25 may be an important mediator of allergic disease via
production of IL-4, IL-5, IL-13, and eotaxin.
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