Homozygous CCR4−/− mice were backcrossed with C57BL/6 mice (Centre d'Elevage Janvier) for four generations. Age- and weight-matched CCR4−/− and CCR4+/+ littermates from heterozygote (CCR4+/−) matings from the fourth backcross were used in this study to control for strain background. Mice (20–25 g) of either sex were immunized intraperitoneally with 10 μg of OVA (A-5503; Sigma-Aldrich) in 0.2 ml of alum (Serva). Control mice received an injection of saline (0.9% wt/vol NaCl) alone. 14 d later, mice were anesthetized by inhaled 2% FORENE™ (Abbott) and 50 μg of OVA was administered to the lungs (in 50 μl of saline) intranasally as described previously 17 . Control mice received 50 μl saline only. This procedure was repeated daily for 5 d. Animals were finally killed by lethal injection of 60 mg/kg pentobarbital. Student's t test was used for statistical analysis, except that for the analysis of the survival curves, we performed the log rank test (two-tailed).
Phenol-extracted bacterial LPS from Escherichia coli 055:B5 (List Biological Laboratories) was administered at 60, 90, and 120 mg/kg intraperitoneally for the high dose LPS shock model. For the low dose LPS shock model, mice received 1, 2, and 4 μg of LPS with 8 mgd -galactosamine (D-gal; Fluka) in 0.5 ml saline. Animals were killed by CO2 asphyxiation at the time points indicated in the figures.
Phenol-extracted bacterial LPS from Escherichia coli 055:B5 (List Biological Laboratories) was administered at 60, 90, and 120 mg/kg intraperitoneally for the high dose LPS shock model. For the low dose LPS shock model, mice received 1, 2, and 4 μg of LPS with 8 mg