Linked Life Data

10571730

Source:http://linkedlifedata.com/resource/pubmed/id/10571730

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1999-12-8
pubmed:abstractText
Psoriasis vulgaris is a skin disease potentially mediated by pro-inflammatory cytokines produced by type 1 lesional T cells. The capability of individual T cells to produce these cytokines in lesional skin is not known. In this study we measured the ability of lesional and peripheral blood T cells to produce intracellular interferon-gamma, tumor necrosis factor-alpha, interleukin-2, interleukin-4, and interleukin-10 proteins as detected by flow cytometric analysis. Cytokine synthesis was induced by activation with ionomycin/phorbol myristate acetate (in the presence of Brefeldin A, which inhibits the exocytosis of these cytokines). After stimulation, we found relatively high percentages of epidermal CD8 and CD4 T cells capable of producing interferon-gamma, tumor necrosis factor-alpha, and interleukin-2, whereas few T cells, < 11%, expressed interleukin-4 or interleukin-10. Hence both CD8+ and CD4+ T cells are capable of type 1 effector functions (TC1 and TH1, respectively). This activation scheme was repeated on peripheral blood T cells from psoriatic patients versus healthy controls, where we also found a type 1 bias. In order to evaluate quantitatively the type 1 cytokine bias, we compared the frequency of type 2 interleukin-4 producing versus type 1 interferon-gamma producing T cells in our assay and found a shift towards type 1 producing cells. This shift reveals a type 1 differentiation bias in both lesional areas and in the peripheral blood, which may indicate an imbalance within the T cell population, which is contributing to the chronic or sustained immunologic activation of T cells found in this disease.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-202X
pubmed:author
pubmed:issnType
Print
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
752-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10571730-Adult, pubmed-meshheading:10571730-Aged, pubmed-meshheading:10571730-CD4-CD8 Ratio, pubmed-meshheading:10571730-Cell Differentiation, pubmed-meshheading:10571730-Cytokines, pubmed-meshheading:10571730-Epidermis, pubmed-meshheading:10571730-Female, pubmed-meshheading:10571730-Humans, pubmed-meshheading:10571730-Interferon-gamma, pubmed-meshheading:10571730-Interleukin-2, pubmed-meshheading:10571730-Ionomycin, pubmed-meshheading:10571730-Lymphocyte Activation, pubmed-meshheading:10571730-Male, pubmed-meshheading:10571730-Middle Aged, pubmed-meshheading:10571730-Psoriasis, pubmed-meshheading:10571730-T-Lymphocytes, pubmed-meshheading:10571730-T-Lymphocytes, Cytotoxic, pubmed-meshheading:10571730-Tetradecanoylphorbol Acetate, pubmed-meshheading:10571730-Th1 Cells, pubmed-meshheading:10571730-Tumor Necrosis Factor-alpha
pubmed:year
1999
pubmed:articleTitle
The majority of epidermal T cells in Psoriasis vulgaris lesions can produce type 1 cytokines, interferon-gamma, interleukin-2, and tumor necrosis factor-alpha, defining TC1 (cytotoxic T lymphocyte) and TH1 effector populations: a type 1 differentiation bias is also measured in circulating blood T cells in psoriatic patients.
pubmed:affiliation
laboratory of Investigative Dermatology, The Rockerfeller University, New York, New York 10021-6399, USA. austinl@rockvax.rockerfeller.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't