Document 0595 DOCN M9620595 TI The effect of 2-acetyl-4-tetrahydroxybutylimidazole on lymphocyte subsets during a contact hypersensitivity response in the NOD mouse. DT 9602 AU Gugasyan R; Losinno C; Mandel T; Walter and Eliza Hall Institute of Medical Research, Parkville,; Victoria, Australia. SO Immunol Lett. 1995 Jun;46(3):221-7. Unique Identifier : AIDSLINE MED/96089928 AB The compound 2-acetyl-4-tetrahydroxybutylimidazole (THI) is known to suppress a contact hypersensitivity (CH) response. The effect of THI on lymphocyte subsets during treatment and in a CH response has not been shown in mice. To further define the immunosuppressive potential of THI, a time-course study during the CH response to oxazolone (OX) was performed. While THI can prevent the induction of CH, if treatment is started before sensitization, it has a low therapeutic capability since it could not significantly inhibit the response when continuous oral treatment was commenced during the course of CH. We report that during this response continuous oral treatment of non-obese diabetic (NOD) mice with THI reduced the number of CD4+ and CD8+ T cells in the peripheral blood. In the draining lymph nodes THI treatment had no effect on lymphocyte subsets prior to contact sensitization, but subsequent sensitization and elicitation with OX could not stimulate a significant increase in the number of CD4+ T cells in the treated mice, whereas untreated control mice showed elevated numbers of these lymphocytes. These findings suggest that THI can inhibit an CH response by preventing the recruitment of CD4+ T cells in the draining lymph nodes through an unknown mechanism. DE Animal Cell Count CD4-Positive T-Lymphocytes/DRUG EFFECTS CD8-Positive T-Lymphocytes/DRUG EFFECTS Dermatitis, Contact/BLOOD/DRUG THERAPY/*IMMUNOLOGY Female Imidazoles/*PHARMACOLOGY/THERAPEUTIC USE Immunosuppressive Agents/*PHARMACOLOGY/THERAPEUTIC USE Lymph Nodes/DRUG EFFECTS Lymphopenia/CHEMICALLY INDUCED Mice Mice, Inbred NOD Support, Non-U.S. Gov't T-Lymphocyte Subsets/*DRUG EFFECTS JOURNAL ARTICLE SOURCE: National Library of Medicine. NOTICE: This material may be protected by Copyright Law (Title 17, U.S.Code).