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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0024264,
umls-concept:C0085358,
umls-concept:C0086418,
umls-concept:C0108789,
umls-concept:C1123023,
umls-concept:C1179149,
umls-concept:C1332714,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1511636,
umls-concept:C1515877,
umls-concept:C1706438,
umls-concept:C1879547,
umls-concept:C2003905,
umls-concept:C2698600
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pubmed:issue |
6
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pubmed:dateCreated |
1988-4-20
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pubmed:abstractText |
In vivo exposure of human epidermis to UV abrogates the function of T6+DR+ Langerhans cells and induces the appearance of Ag-presenting T6-DR+ OKM5+ cells in the epidermis. Since UV exposure of murine skin results in Ts lymphocyte activation, we investigated the capacity of human epidermal cells (EC) harvested 3 days after in vivo UV exposure to activate regulatory and effector autologous T lymphocyte subsets. T lymphocytes were separated into CD8+ suppressor/cytotoxic lymphocytes and CD4+ helper/inducer lymphocytes by C lysis and panning. The CD4+ subset was further divided by using the 2H4 mAB to obtain CD4+2H4+ lymphocytes (inducers of TS lymphocytes) and CD4+2H4- lymphocytes (inducers of B cell Ig production and inducers of cytotoxic T cells). Unirradiated suction blister-derived EC from control skin (C-EC) and from skin exposed in vivo to UV (UV-EC) were cultured with purified autologous T lymphocyte subsets in the absence of added Ag. The resultant T lymphocyte proliferation was detected by [3H]thymidine uptake. UV-EC were highly effective in the stimulation of CD4+ lymphocytes, whereas C-EC were poor stimulators. The stimulator effect of UV-EC was abrogated after depletion of DR+ UV-EC. When CD4+ lymphocytes were fractionated, UV-EC consistently demonstrated enhanced ability to stimulate suppressor-inducer CD4+2H4+ lymphocytes relative to C-EC. Although less responsive than CD4+2H4+ lymphocytes, CD4+2H4- lymphocytes also demonstrated greater proliferation to UV-EC than to C-EC. Neither UV-EC nor C-EC were able to activate CD8+ lymphocytes devoid of CD4+ lymphocytes. However, after addition of rIL-2 at concentrations that allow binding only to the high affinity IL-2R on T lymphocytes, UV-EC induced vigorous proliferation of CD8+ lymphocytes, whereas C-EC induced only background levels of proliferation. C lysis of leukocytes resident within UV-EC resulted in 66 to 70% reduction of CD8+ lymphocyte proliferation. In conclusion, UV-EC may activate CD8+ lymphocytes by at least two pathways: (1) UV-EC activation of CD4+2H4+ lymphocytes may induce differentiation/proliferation of CD8+ suppressor cells and (2) UV-EC activation of CD4+ cells may induce IL-2 production, that, in combination with UV-induced epidermal leukocytes, stimulates CD8+ cells.
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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 |
Mar
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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 |
140
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1738-44
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:2964481-Adult,
pubmed-meshheading:2964481-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:2964481-Cell Division,
pubmed-meshheading:2964481-Epidermis,
pubmed-meshheading:2964481-Humans,
pubmed-meshheading:2964481-Interleukin-2,
pubmed-meshheading:2964481-Lymphocyte Activation,
pubmed-meshheading:2964481-T-Lymphocytes, Cytotoxic,
pubmed-meshheading:2964481-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:2964481-T-Lymphocytes, Regulatory,
pubmed-meshheading:2964481-Ultraviolet Rays
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pubmed:year |
1988
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pubmed:articleTitle |
Human epidermal cells from ultraviolet light-exposed skin preferentially activate autoreactive CD4+2H4+ suppressor-inducer lymphocytes and CD8+ suppressor/cytotoxic lymphocytes.
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pubmed:affiliation |
Department of Dermatology, University of Michigan Medical School, Ann Arbor Veterans Administration Hospital, MI 48109.
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, U.S. Gov't, Non-P.H.S.,
Research Support, Non-U.S. Gov't
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