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200 of OVA-challenged wild-type, IL-4-deficient, and IL-4Rα-deficient mice were 0.24 ± 0.025, 0.36 ± 0.026, and 0.45 ± 0.058 mg/kg, respectively.
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After subcutaneous priming with OVA on days -14 and -7, BALB/c wild-type mice were administered intranasally 55 μl of IL-13R-FC (13) or immunoglobulin control protein (Ig control) in phosphate-buffered saline (PBS). We administered 110 μg of IL-13R-Fc on days 0, 1, 2, 3, 3.5, 4, and 4.5, and 110 μg of Ig control was given on days 0.1,2, and 4. Both proteins were administered with 750 μg of OVA on days 1,2, and 4. Data were collected on day 5 (9).
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-/- mice were administered 3 to 5 μg of recombinant IL-4 or IL-13, or control protein (bovine serum albumin or irrelevant rat antibody) intranasally on days 1, 3, and 5, and data were collected 12 to 15 hours later (9). For clarity, only data from BALB/c wild-type mice are shown.
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7 washed cells intravenously. The mice were challenged intranasally with OVA for 6 consecutive days. Data were collected on day 7 (9).
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We thank D. Erle, M. Wills-Karp, R. Coffman, and F. Finkelman for helpful discussions, the Research Support Team of Genetics Institute for IL-13Rα2-Fc protein, and R. Coffman for IL-4. Supported by NIH grants T32 HL07185 (G.G.), 03344 (D.B.C), 47412, 53949, 33259 (D.S.), 09883 (R.V.), and P01-HL56385; the Crohn's and Colitis foundation and the Hefni Scholars Fund (A.E.W.); Howard Hughes Medical Institute (M.M. and R.M.L); and Schering-Plough Corporation (D.M.R.).
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