Immunity to herpes simplex virus type 2: viral antigen-presenting capacity of epidermal cells and its impairment by ultraviolet irradiation.
Ia+ epidermal cells (EC) had accessory cell function for herpes simplex virus type 2 (HSV-2)-induced T cell proliferation of immune lymph node cells (LNC). The EC-mediated virus-induced proliferative response of immune LNC was inhibited by ultraviolet B (UVB) irradiation. When EC were pulsed with viral antigen before UVB irradiation, the response was partially restored by addition of epidermal cell-derived thymocyte-activating factor (ETAF). Although normal EC secreted prostaglandin E2, the levels secreted by UVB-irradiated EC were significantly reduced, and the UVB-induced suppression of the proliferative response of immune LNC was not corrected by indomethacin. Soluble factor(s) that suppresses proliferation was generated in supernatants from cultures containing UVB-irradiated but not nonirradiated EC. Sephadex chromatography revealed the presence of factors differentially modulating the proliferative response of HSV-stimulated immune LNC and concanavalin A-stimulated normal lymphoid cells.
D000818:Animals; D000938:Antigen-Presenting Cells / Q000276:immunology* / Q000528:radiation effects; D000956:Antigens, Viral / Q000276:immunology*; D004817:Epidermis / Q000276:immunology* / Q000378:metabolism / Q000528:radiation effects; D005260:Female; D006801:Humans; D007213:Indomethacin / Q000494:pharmacology; D008198:Lymph Nodes / Q000166:cytology; D008213:Lymphocyte Activation / Q000187:drug effects / Q000528:radiation effects*; D051379:Mice; D008807:Mice, Inbred BALB C; D011458:Prostaglandins E / Q000037:antagonists & inhibitors; D018139:Simplexvirus / Q000276:immunology*; D013491:Suppressor Factors, Immunologic / Q000096:biosynthesis; D014466:Ultraviolet Rays
D000956:Antigens, Viral; D011458:Prostaglandins E; D013491:Suppressor Factors, Immunologic; D007213:Indomethacin