Immune Netw.  2002 Jun;2(2):65-71. 10.4110/in.2002.2.2.65.

Immunologic Mechanism of Experimental and Therapeutic Ultraviolet B Responses

• Lew W

• KMID: 1571484
• DOI: http://doi.org/10.4110/in.2002.2.2.65

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.

Keyword

Ultraviolet B; contact hypersensitivity; delayed type hypersensitivity; infection; immune suppression; apoptosis

MeSH Terms

Animals
Antibodies, Blocking
Apoptosis
Cytokines
Dermatitis, Contact
Hypersensitivity
Interleukin-10
Macrophages
Mice
Mice, Knockout
Phagocytosis
Psoriasis
Skin Diseases
T-Lymphocytes
Antibodies, Blocking
Cytokines
Interleukin-10