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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
2
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pubmed:dateCreated |
1991-2-19
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pubmed:abstractText |
We have recently demonstrated that a single dose (200 J/m2) of UVB radiation abrogates the capacity of mouse epidermal Langerhans cells (LC) or splenic adherent cells (SAC) to present keyhole limpet hemocyanin (KLH) to Ag-specific, MHC-restricted CD4+ Th1 cells. In the present study we determined whether such Th1 unresponsiveness represented long-lasting immunologic tolerance. To address this question, Th1 were preincubated with KLH-pulsed UVB-LC or UVB-SAC, then isolated and restimulated with unirradiated APC (LC or SAC) plus KLH or with exogenous rIL-2 in the absence of APC. Preincubation with KLH and UVB-LC or UVB-SAC rendered Th1 unresponsive to subsequent restimulation with APC and KLH. In addition, such Th1 were defective in their autocrine IL-2 production, but could respond normally to exogenous rIL-2, indicating that unresponsiveness was due to functional inactivation and not to cell death. Th1 unresponsiveness was Ag-specific, MHC-restricted, and long lasting (greater than 16 days). In addition, it appears that Th1 unresponsiveness is not due to the release of soluble suppressor factors from UVB-LC or UVB-SAC because supernatants from such cells had no effect on Th1 proliferation. Addition of unirradiated allogeneic SAC during preincubation prevented the induction of unresponsiveness by UVB-LC or UVB-SAC, suggesting that UVB interferes with the capacity of LC or SAC to deliver a costimulatory signal(s) that can be provided by allogeneic SAC. We conclude that UVB can convert LC or SAC from immunogenic to tolerogenic APC.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
146
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
485-91
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:1670944-Animals,
pubmed-meshheading:1670944-Antigen-Presenting Cells,
pubmed-meshheading:1670944-CD4-Positive T-Lymphocytes,
pubmed-meshheading:1670944-Dose-Response Relationship, Radiation,
pubmed-meshheading:1670944-Female,
pubmed-meshheading:1670944-Hypersensitivity, Delayed,
pubmed-meshheading:1670944-Immune Tolerance,
pubmed-meshheading:1670944-Interleukin-2,
pubmed-meshheading:1670944-Langerhans Cells,
pubmed-meshheading:1670944-Mice,
pubmed-meshheading:1670944-Mice, Inbred BALB C,
pubmed-meshheading:1670944-Mice, Inbred C3H,
pubmed-meshheading:1670944-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:1670944-Time Factors,
pubmed-meshheading:1670944-Ultraviolet Rays
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pubmed:year |
1991
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pubmed:articleTitle |
Ultraviolet B radiation converts Langerhans cells from immunogenic to tolerogenic antigen-presenting cells. Induction of specific clonal anergy in CD4+ T helper 1 cells.
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pubmed:affiliation |
Department of Dermatology, University of Texas Southwestern Medical Center, Dallas 75235.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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