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J. Exp. Med.,
Volume 189, Number 10, May 17, 1999 1565-1572
By
From the * Medical Research Council Laboratory of Molecular Biology, Hills Road, Cambridge
CB2 2QH, United Kingdom; the Using a single vector targeting strategy, we have generated mice with a combined deficiency of
interleukin (IL)-4 and IL-13 to clarify their roles in T helper type 2 (Th2) cell responses. Using
immunological challenges normally characterized by a Th2-like response, we have compared
the responses of the double-deficient mice with those generated by wild-type, IL-4-deficient,
and IL-13-deficient mice. Using a pulmonary granuloma model, induced with Schistosoma mansoni eggs, we demonstrate that although eosinophil infiltration, immunoglobulin E, and IL-5
production are reduced in the IL-4-deficient mice and IL-13-deficient mice, they are abolished only in the combined absence of both cytokines. Furthermore, IL-4/13-deficient animals
are severely impaired in their ability to expel the gastrointestinal nematode Nippostrongylus brasiliensis. Unexpectedly, N. brasiliensis-infected IL-4/13-deficient mice developed elevated IL-5
and eosinophilia, indicating that compensatory mechanisms exist for the expression of IL-5, although serum IgE remained undetectable. IL-4/13-deficient mice default to a Th1-like phenotype characterized by the expression of interferon Department of Pathology, University of Cambridge, Cambridge
CB2 1QP, United Kingdom; and the § School of Biological Sciences, University of Manchester,
Manchester M13 9PT, United Kingdom
and the production of IgG2a and IgG2b.
We conclude that IL-4 and IL-13 cooperate to initiate rapid Th2 cell-driven responses, and
that although their functions overlap, they perform additive roles.
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