KONDO, S and WANG, BH and FUJISAWA, H and SHIVJI, GM and ECHTENACHER, B and MAK, TW and SAUDER, DN (1995) EFFECT OF GENE-TARGETED MUTATION IN TNF RECEPTOR (P55) ON CONTACT HYPERSENSITIVITY AND ULTRAVIOLET B-INDUCED IMMUNOSUPPRESSION. JOURNAL OF IMMUNOLOGY, 155 (8). pp. 3801-3805. ISSN 0022-1767,
Full text not available from this repository.Abstract
Tumor necrosis factor alpha (TNF-alpha) is a pleiotropic proinflammatory cytokine. TNF-alpha has been implicated in the pathogenesis of delayed-type hypersensitivity reactions such as allergic contact hypersensitivity and has been suggested as a mediator of ultraviolet B (UVB)-induced immunosuppression. Conflicting reports, however, exist concerning the effects of TNF-alpha on contact hypersensitivity (CHS). To determine the role of TNF-alpha in the generation and regulation of CHS, gene-targeted mutant mice lacking TNF-receptor (p55) gene (TNF-R1(-) mice) were treated with dinitrofluorobenzene (DNFB) to induce CHS. TNF-R1(-) mice showed significant hyperresponsiveness in CHS (152.8 +/- 20.9%, p < 0.025) compared with normal syngeneic mice (C57BL/6) assessed by ear swelling. To determine whether UVB can Induce suppression in TNF-R1(-) mice, mice were irradiated on the shaved abdomen with 96 mJ/cm(2) UVB and 3 days later they were painted with 0.5% DNFB (sensitization dose); followed 5 days later with 0.2% DNFB to the left ear (challenge dose). Significant suppression of CHS was observed both locally (sensitization on irradiated site) and systemically (sensitization on unirradiated site) in UVB-irradiated TNF-R1(-) mice as well as in normal mice. To rule out possible signaling through p75 TNF-R, the mice were treated with anti-TNF-alpha Ab (V1q), which can neutralize any TNF effects through either receptor. V1q had no effect on these phenomena observed in TNF-R1(-) mice. These results suggest that TNF-alpha plays a regulatory role in CHS but is not required to induce UVB-mediated immunosuppression.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TUMOR-NECROSIS-FACTOR; FACTOR-ALPHA; CUTANEOUS IMMUNITY; UROCANIC ACID; LIGHT-B; MICE; RADIATION; SUPPRESSION; EXPRESSION; EXPOSURE; |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:37 |
| URI: | https://pred.uni-regensburg.de/id/eprint/52269 |
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