To elucidate the sensitization mechanism of allergic contact dermatitis isolation of carrier substances from DNCB-treated epidermis was attempted. The homogenate of the epidermis was found to contain immunogenic substances. One of its subcellular fractions could elicit intense contact hypersensitivity although it contained less amounts of haptenic groups than other fractions. Electron microscopy revealed it to be the microsomal fraction of epidermal cells. Treatment of the fraction with deoxycholic acid caused slight reduction of its immunizing ability.
The migration inhibitory factor (MIF) production of peripheral lymphocytes following exposure to dinitrophenylated microsomes derived from both human (DNP-hy-Mic) and guinea pig (DNP-gp-Mic) epidermis was quantitated to detect human contact sensitivity to dinitrochlorobenzene (DNCB). The lymphocytes from nonsensitized subjects did not generate MIF following exposure to either antigen. With DNP-gp-Mic as the antigen, MIF production was noted in only 1 out of 6 DNCB-sensitized subjects and was not significant statistically. With DNP-hu-Mic as the antigen, highly significant MIF production was observed in all 12 sensitized subjects ( p less than 0.0005). In order to confirm MIf production by sensitized lymphocytes following stimulation by DNP-hu-Mic, the subjects were actively sensitized with DNCB and MIF production was assessed before and after sensitization. Remarkable MIf production was noted in the lymphocyte cultures after sensitization, although no significant MIF production was observed before sensitization. MIF production of the sensitized lymphocytes cultured in the presense of DNP-hu-Mic generally correlated well with the results of patch testing, but not with the intensity of the skin test.
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