Immunologic Mechanism of Experimental and Therapeutic Ultraviolet B Responses.
- Author:
Wook LEW
1
Author Information
- Publication Type:Original Article
- Keywords: Ultraviolet B; contact hypersensitivity; delayed type hypersensitivity; infection; immune suppression; apoptosis
- MeSH: Animals; Antibodies, Blocking; Apoptosis; Cytokines; Dermatitis, Contact; Hypersensitivity; Interleukin-10; Macrophages; Mice; Mice, Knockout; Phagocytosis; Psoriasis; Skin Diseases; T-Lymphocytes
- From:Immune Network 2002;2(2):65-71
- CountryRepublic of Korea
- Language:English
- Abstract: The immunological mechanism of the responses to ultraviolet (UV) B radiation in mouse models were investigated by the suppression of contact hypersensitivity (CHS) and delayed type hypersensitivity (DTH), and susceptibility to infection. However, there are some differences in immune suppression according to the different models as well as the irradiation protocols. Therefore, this review focused on the differences in the suppressive effects on CHS and DTH, and susceptibility to infection in relation to the different in vivo models. Recent advances in cytokine knockout mice experiments have the reexamination of the role of the critical cytokines in UVB-induced immune suppression, which was investigated previously by blocking antibodies. The characteristics of the suppressor cells responsible for UVB-induced tolerance were determined. The subcellular mechanism of UVB-induced immune suppression was also explained by the induction of apoptotic cells through the Fas and Fas-ligand interaction. The phagocytosis of the apoptotic cells is believed to induce the production of the immune suppressive cytokine like interleukin-10 by macrophages. Therefore, the therapeutic UVB response to a skin disease, such as psoriasis, by the depletion of infiltrating T cells could be considered in the extension line of apoptosis and immune suppression.
