title: CD4+ T cells in lymph nodes of UVB-irradiated mice suppress immune responses to new antigens both in vitro and in vivo.
abstract: The mechanisms by which erythemal UVB irradiation modulates systemic immune responses to antigens applied to non-irradiated sites are poorly understood. In this study, regulatory CD4+ T cells were identified in the skin-draining lymph nodes (SDLNs) of UVB-irradiated, but otherwise naive mice. A transgenic mouse strain (DO11.10) was utilized in which the majority of CD4+ T cells expressed the ovalbumin (OVA(323-339)) T-cell receptor. Thus, T-cell responses could be examined following erythemal UVB irradiation without further antigen sensitization. CD4+ T cells from the SDLNs of UVB-irradiated mice had significantly reduced capacity to respond to presentation of the OVA(323-339) peptide in vitro. Transfer of CD4+ T cells from the SDLNs of UVB-irradiated antigen-naive mice significantly reduced both OVA sensitization and contact hypersensitivity responses to an experimental hapten in the recipient mice. Depletion of CD4+CD25+ cells abrogated this UVB-suppressive effect in the in vitro proliferation assay. There was also a significant increase in the proportion of CD4+CD25+Foxp3+ cells in the SDLNs of UVB-irradiated mice. The potential of these regulatory cells poised to regulate responses to incoming antigens at distant non-irradiated sites broadens the biological impact of UVB irradiation of skin on immunity.
authors.affiliation: Telethon Institute for Child Health Research, Centre for Child Health Research, University of Western Australia, Perth, Western Australia, Australia.
authors.forename: Shelley
authors.initials: S
authors.lastname: Gorman
authors.forename: Jamie W-Y
authors.initials: JW
authors.lastname: Tan
authors.forename: Stephanie T
authors.initials: ST
authors.lastname: Yerkovich
authors.forename: John J
authors.initials: JJ
authors.lastname: Finlay-Jones
authors.forename: Prue H
authors.initials: PH
authors.lastname: Hart
mesh_terms: D000818:Animals; D000917:Antibody Formation / Q000502:physiology*; D000941:Antigens / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000166:cytology / Q000378:metabolism / Q000502:physiology* / Q000528:radiation effects*; D049109:Cell Proliferation; D002478:Cells, Cultured; D003877:Dermatitis, Contact / Q000517:prevention & control; D004307:Dose-Response Relationship, Radiation; D051858:Forkhead Transcription Factors / Q000378:metabolism; D007114:Immunization; D053645:Interleukin-2 Receptor alpha Subunit / Q000378:metabolism; D008198:Lymph Nodes / Q000166:cytology*; D051379:Mice; D008807:Mice, Inbred BALB C; D008822:Mice, Transgenic; D010047:Ovalbumin / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D010446:Peptide Fragments / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000378:metabolism; D013997:Time Factors; D014466:Ultraviolet Rays
chemical_list: D000941:Antigens; D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D053645:Interleukin-2 Receptor alpha Subunit; C111390:OVA 323-339; D010446:Peptide Fragments; D011948:Receptors, Antigen, T-Cell; D010047:Ovalbumin