The 'dapsone syndrome' developed in a 44-year-old woman who was treated for pyoderma gangrenosum with 100 mg/day dapsone for about 5 weeks. Symptoms included fever, malaise, jaundice with hepatic dysfunction, lymphadenopathy, mononucleosis and dermatitis. These symptoms disappeared with 30 mg/day of oral prednisolone. A lymphocyte stimulation test with dapsone was positive, as was the delayed-type intradermal skin test with 0.5 and 0.05% dapsone in saline. Immunohistochemical studies of the rash and skin test reaction revealed that the dominant infiltrating T cells in the upper dermis were of the Leu 2a+ cytotoxic/suppressor-type rather than the Leu 3a+ helper/delayed hypersensitivity-type.
As a first step in determining the genetic control of contact hypersensitivity in mice, 2,4-dinitro-1-fluorobenzene (DNFB) was applied to induce ear swellings. Studies with congenic and recombinant inbred strains of mice revealed that the DNFB contact hypersensitivity is controlled by the I-A subregion, as well as non-H-2 regions. The results presented suggest that the major histocompatibility complex-linked immune response genes seem to be playing an important role in the contact hypersensitivity to the DNFB antigen.
Suppressor T cells (Ts) induced by lysozyme-modified syngeneic lymphocytes were characterized. Hen egg-white lysozyme (HEL)-specific delayedtype hypersensitivity (DTH) was suppressed when HEL-induced Ts were transferred into naive mice. These HEL-induced Ts had surface markers of both Thy-l antigen, and I-] gene products. The suppression of HEL-specific DTH was greatly increased, when these Ts had been enriched with HEL-coated petri dishes.Isolated anti-HEL antibodies from BIO.BR or A/Sn mice were inoculated into rabbits to induce anti-cross-reactive idiotype (CRI) antibodies. The rabbit antisera were extensively absorbed with normal BlO.BR or A/Sn immunoglobulins (Igs) and MOPC 104E ascites Igs to render them idiotype (Id) specific. Using these anti-CRI antibodies, we observed that these Ts possessed Id receptors on their cell surface. Results of both fluorescence techniques and cytotoxicity tests revealed that about 10% of the enriched T cells containing these Ts were Id positive. Moreover, these enriched T cells were substantially killed by anti-I-] antiserum plus complement. However, this killing was completely blocked by HEL antigen. These results suggest that both Id receptors and I-] gene products might be forming the same molecular complexes or might coexist in the vicinity of the molecule.
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