Attenuation of IC-induced lung injury by C5aR and FcγRIII deficiency. C57BL/6 WT (filled circles), FcγRIII–/– (filled squares), and C5aR–/– (filled triangles) mice received 150 μg anti-OVA Ab intratracheally and 20 mg/kg OVA Ag intravenously, and the inflammatory response in the lung was allowed to proceed for 2 to 24 hours (IC). Mice not receiving OVA Ag served as Ab controls (open circles). At the indicated times, mice were killed, and PMN accumulation in lung tissue (a), PMN influx in the alveolar space (b), and hemorrhage (c), were evaluated. The results are expressed as means ± SEM (n = 7–18 mice for each group). Differences for hemorrhage and alveolar and interstitial PMN infiltration were significant (P < 0.05) for the IC treatment groups of WT mice as compared with FcγRIII–/– and C5aR–/– mice at 4, 8, and 24 hours. FcγRIII–/– and C5aR–/– mice only differed significantly for alveolar PMN accumulation (see text). Ab control values do not differ between WT, FcγRIII–/–, and C5aR–/– mice (data not shown).