Primary defect in UVB-induced systemic immunomodulation does not relate to immature or functionally impaired APCs in regional lymph nodes

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dc.contributor.authorGorman, S.
dc.contributor.authorTan, J.
dc.contributor.authorThomas, J.
dc.contributor.authorTownley, S.
dc.contributor.authorStumbles, P.
dc.contributor.authorFinlay-Jones, J.
dc.contributor.authorHart, P.
dc.date.issued2005
dc.descriptionCopyright © 2005 by The American Association of Immunologists, Inc.
dc.description.abstractUVB irradiation of the shaved dorsal skin of mice can cause both local and systemic suppression of contact hypersensitivity responses; the former demonstrated by administration of the sensitizing Ag/hapten to the irradiated site and the latter by its administration at least 72 h later to distal unirradiated sites. The immunological basis of systemic immunomodulation is not clear. When haptens (trinitrochlorobenzene, FITC) were administered to the shaved ventral skin 4 days after irradiation (8 kJ/m(2)) to the shaved dorsum of BALB/c mice, CD11c(+)/FITC(+) cells in the skin-draining lymph nodes from control and irradiated mice produced on a per cell basis similar levels of IL-12 and PGE(2) were phenotypically mature and efficient at presenting FITC to lymphocytes from FITC-sensitized mice. Ag presentation by FACS-sorted CD11c(+) lymph node cells isolated 4 days after UVB irradiation was as efficient as were cells from unirradiated mice at presentation in vitro of an OVA peptide (OVA(323-339)) to CD4(+) cells from OVA-TCR-transgenic DO11.10 mice. Further, IFN-gamma levels were increased in the cultures containing CD11c(+) cells from UVB-irradiated mice, suggesting that inflammation may precede downstream immunosuppression. These results suggest that the primary cause of reduced contact hypersensitivity responses in mice in which UV irradiation and the sensitizing Ag are applied to different sites several days apart must originate from cells other than CD11c(+) APCs that directly or by production of soluble mediators (IL-12, PGE(2)) affect cellular responses in the nodes of UVB-irradiated mice.
dc.description.statementofresponsibilityShelley Gorman, Jamie W.-Y. Tan, Jennifer A. Thomas, Scott L. Townley, Philip A. Stumbles, John J. Finlay-Jones and Prue H. Hart
dc.identifier.citationJournal of Immunology, 2005; 174(11):6677-6685
dc.identifier.doi10.4049/jimmunol.174.11.6677
dc.identifier.issn0022-1767
dc.identifier.issn1550-6606
dc.identifier.urihttp://hdl.handle.net/2440/45328
dc.language.isoen
dc.publisherAmer Assoc Immunologists
dc.source.urihttp://www.jimmunol.org/cgi/content/abstract/174/11/6677
dc.subjectLymph Nodes
dc.subjectAntigen-Presenting Cells
dc.subjectDendritic Cells
dc.subjectSkin
dc.subjectAnimals
dc.subjectMice, Inbred BALB C
dc.subjectMice, Transgenic
dc.subjectMice
dc.subjectDermatitis, Contact
dc.subjectPicryl Chloride
dc.subjectFluorescein-5-isothiocyanate
dc.subjectDinoprostone
dc.subjectInterleukin-12
dc.subjectImmunologic Factors
dc.subjectHaptens
dc.subjectCoculture Techniques
dc.subjectAdministration, Topical
dc.subjectUltraviolet Rays
dc.subjectCell Differentiation
dc.subjectCell Movement
dc.subjectAntigen Presentation
dc.subjectAmino Acid Sequence
dc.subjectMolecular Sequence Data
dc.subjectFemale
dc.subjectCD11c Antigen
dc.titlePrimary defect in UVB-induced systemic immunomodulation does not relate to immature or functionally impaired APCs in regional lymph nodes
dc.typeJournal article
pubs.publication-statusPublished

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