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KMID : 0357119980200040459
Korean Journal of Immunology
1998 Volume.20 No. 4 p.459 ~ p.466
The Effects of Korean Medical Drug on Lymphocyte Activity in Allergic Contact Dermatitis
Á¤¹ÎÈ£/1Soo-Jin Jung
2Jong-Hwa Lee/2Yeon-Hee Kim/2Young-Jin Lim/2Min-Ho Jeong/3Sung Tae Yee/4Sang-Hyun Ahn/4In-Sick Park/4Jin-Taek Kim
Abstract
The purpose of this study was to elucidate the effects of Hwangyun, Hwangyunhaedogtang, and Kumeunhwa on the lymphocyte activity in allergic contact dermatitis induced by contact allergen 1-chloro-2,4-dinitrobenzene (DNCB) of Balb/c mouse. For examination of a contact hypersensitivity, MEST (mouse ear swelling test) and lymphocyte proliferation assay measured by [(3)H]-methylthymidine incorporation were done. Cytokine mRNA in the draining lymph node cells were examined by RT-PCR. Contact hypersensitivity was more effectively induced by 0.25% DNCB treatment than 1% DNCB treatment. Local lymph node cell proliferation from DNCB-sensitized mouse was most highly elicitated with 100 ug/ml DNBS stimulation in vitro. The cytokine profiles of lymph node cells from DNCB-sensitized and DNBS-stimulated mouse were strong expression of IL-2 and IFN-r, weak expression of LT and IL-4, and no expression of IL-6 and IL-10. This lymphocyte proliferation was significantly inhibited in mice administered Korean medical drug for 10 days and sensitized with DNCB at day 5 (88.22%, 65.14%, and 52.29% in Hwangyun, Hwangyunhaedogtang, and Kumeunhwa, respectively). But Kumeunhwa was not effective in the inhibition of lymphocyte proliferation when administered after DNCB-sensitization. The cytokine expressions were also inhibited especially IL-2 and IFN-r in Hwangyun administered- mice. These inhibitions of lymphocyte activity by Korean medical drugs were also observed when stimulated with ConA (1 ug/ml). Conclusively, immune responses of contact hypersensitivity induced by DNCB are involved in local lymph node T cells mainly Th1 type cells, and Korean medical drugs especially Hwangyun suppressed allergic contact dermatitis via inhibition of the activity of these cells.
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