Figure 2
Figure 2. Impaired TNCB-specific DTHRs in TNFR1−/− mice. (A) TNCB-sensitized and naive TNFR1−/− () and TNFR1+/+ (■) mice were challenged with TNCB. Ear thickness was measured before and at the indicated time points after TNCB challenge. Differences in ear thickness between TNFR1−/− () and TNFR1+/+ (■) were significant (P < .05) 24, 48, and 72 hours after ear challenge (24 hours: n = 16-27; 48 hours and 72 hours: n = 6 or 7). (B) Reduced PMN infiltrates, tissue necrosis, and edema in ear tissue from TNFR1−/− mice 24 hours after TNCB challenge. Hematoxylin and eosin–stained ear sections from TNFR1+/+ (left: top represents overview; bottom represents detail) and TNFR1−/− mice (right: top represents overview; bottom represents detail; n = 13-15). (C) PMN recruitment is TNFR1-dependent. MPO activity in protein extracts from ear tissue from TNFR1−/− and TNFR1+/+ mice (n = 3).

Impaired TNCB-specific DTHRs in TNFR1−/− mice. (A) TNCB-sensitized and naive TNFR1−/− () and TNFR1+/+ (■) mice were challenged with TNCB. Ear thickness was measured before and at the indicated time points after TNCB challenge. Differences in ear thickness between TNFR1−/− () and TNFR1+/+ (■) were significant (P < .05) 24, 48, and 72 hours after ear challenge (24 hours: n = 16-27; 48 hours and 72 hours: n = 6 or 7). (B) Reduced PMN infiltrates, tissue necrosis, and edema in ear tissue from TNFR1−/− mice 24 hours after TNCB challenge. Hematoxylin and eosin–stained ear sections from TNFR1+/+ (left: top represents overview; bottom represents detail) and TNFR1−/− mice (right: top represents overview; bottom represents detail; n = 13-15). (C) PMN recruitment is TNFR1-dependent. MPO activity in protein extracts from ear tissue from TNFR1−/− and TNFR1+/+ mice (n = 3).

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