Fig. 3.
Fig. 3. Contact hypersensitivity reactions are compromised in GM-CSF/IL-3–deficient mice. / Mice were sensitized with oxazolone on the abdomen and foot pads on day 0 and challenged on the ear on day 5. Ear thickness was measured with a micrometer. (A) Wild-type versus IL-3–deficient,P < .0001. GM-CSF/IL-3 deficient versus IL-3 deficient,P < .0001. Similar results were observed in 8 independent experiments on both the C57Bl/6 and Balb/c backgrounds. (B) Defective contact hypersensitivity reactions can be reversed by the administration of GM-CSF and IL-3 protein during initial sensitization. Wild-type versus GM-CSF/IL-3 deficient, P < .0001. GM-CSF/IL-3 deficient versus control treatment, not significant. GM-CSF/IL-3 deficient versus GM-CSF/IL-3 treatment,P < .0001. Wild-type versus GM-CSF/IL-3 treatment, not significant. Similar results were observed in 5 independent experiments.

Contact hypersensitivity reactions are compromised in GM-CSF/IL-3–deficient mice.

Mice were sensitized with oxazolone on the abdomen and foot pads on day 0 and challenged on the ear on day 5. Ear thickness was measured with a micrometer. (A) Wild-type versus IL-3–deficient,P < .0001. GM-CSF/IL-3 deficient versus IL-3 deficient,P < .0001. Similar results were observed in 8 independent experiments on both the C57Bl/6 and Balb/c backgrounds. (B) Defective contact hypersensitivity reactions can be reversed by the administration of GM-CSF and IL-3 protein during initial sensitization. Wild-type versus GM-CSF/IL-3 deficient, P < .0001. GM-CSF/IL-3 deficient versus control treatment, not significant. GM-CSF/IL-3 deficient versus GM-CSF/IL-3 treatment,P < .0001. Wild-type versus GM-CSF/IL-3 treatment, not significant. Similar results were observed in 5 independent experiments.

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