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KMID : 0371919910040010107
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Journal of Wonju College of Medicine
1991 Volume.4 No. 1 p.107 ~ p.119
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The Study of Contact Hypersensitivity Suppression Induced by Ultraviolet A Irradiation
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Abstract
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The immunologic consequences of cutaneous ultraviolet B(UVB) radiation exposure have recently received considerable attention, in both human and laboratory animal studies. In mice, chronic exposure to UVB induces and promotes the growth of skin cancer, and pretreatment with UVB also prevents mice from processing epicutaneously applied hapten during the induction of contact hypersensitivity. Irradiation_ with high-does UVB results in systemic suppression while exposure to low-dose UVB results in local suppression. Psoralen ultraviolet A (PUVA) can also induce similar immunosuppression.
However little or no evidence of the immunosuppression has been noted following ultraviolet A(UVA) exposure. The less energetic UVA penetrates deeper into the epidermis and down to the mid and lower dermis. Direct damage to Langerhans cells, dermal capillaries and other dermal components has been found following large doses of UVA exposure.
To study the effects of large doses of UVA irradiation on contact hypersensitivity change and its action mechanism in mice, the change of contact hypersenitivity depending on the dose of UVA, the change of contact hypersensitivity in recipient mice following lymph node cell transfer from UVA. treated donor mice and the changes in the Langerhans cell count after UVA exposure were evaluated.
The results are summarized as follows;
1. With 2-4-dinitro-l-fluorbenzene(DNFB) painting of the UVA(100 J/cmz, 200 J/cmz) irradiated site, local suppression of contact byperasenitivity was observed However, 50 J/cmz of irradiation did not induce any significant local suppression of contact hypersensitivity.
2._With painting of the UVA non-irradiated site, systemic suppression of contact hypersensitivity was observed in the 400 J/cmz, 600 J/cmz and 800 J/cmz irradiated groups. However, 200 J /cmZ irradiation did not induce any significant suppression of contact hypersensitivity.
3. Regarding lymph node cells transfer from UVA treated mice with DNFB painting of the non-irradiated site. However no contact hypersensitivity was observed in recipient mice recieving lymph node cells from donor mice with DNFB painting of the irradiated site.
4. With respect to numeric changes of the epidermal Langerhans cells after UVA exposure, decrease in the Langerhans cell count started 4 days after 50 J/cmz of irradiation 1 day after 100 J/cmz or more irradiation in a dose dependent manner. There was no recovery of the Langerhans cell count until 10 days after the UUVA exposure.
From the above results, it maybe´ concluded that the epidermal -Langerhans cell count in mice decreased after a high dose of UVA exposure. Local suppression of contact hypersensitivity was observed when was painted on the irradiated site. This suggested that a decreased Langerhans cell causes count local suppression.´ Considering the results of the systemic suppression and lymph node cell transfer tests, the main cause of systemic suppression of contat hypersensitivity in mice after high dose of UVA exposure appears not to be the change of the effector cell in the lymph node but the skin which inhibit the efferent pathways of contact hypersensitivity.
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