Linked Life Data

1588126

Source:http://linkedlifedata.com/resource/pubmed/id/1588126

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6 Suppl
pubmed:dateCreated
1992-6-25
pubmed:abstractText
A principal mechanism by which ultraviolet (UV) B radiation exerts its selective and antigen-specific suppressive influence on immune responses is through its effects on the capacity of antigen-presenting cells (APC) in skin, primarily Langerhans cells (LC), to differentially activate T-cell subsets. Recent evidence has indicated that LC, following UVB radiation, lose the capacity to stimulate proliferation of CD4+ Th1, but not of Th2, clones. Additional work has shown this acquired unresponsiveness of Th1 cells to represent a long-lasting form of clonal anergy that results from a block in their ability to produce IL-2. Although not completely delineated, these defects appear to be the result of preserved delivery of the primary signal transduced by interaction of the MHC/antigen complex on APC with the T-cell receptor complex, in the absence of a viable second signal normally delivered by interaction of a co-stimulatory factor from APC with its appropriate ligand on the T cells. These findings support the notion that the outcome of certain immune responses depends greatly upon conditions that are brought to bear on APC and T cells during the time of antigen presentation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-202X
pubmed:author
pubmed:issnType
Print
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
66S-69S
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1992
pubmed:articleTitle
Ultraviolet B-irradiated antigen-presenting cells display altered accessory signaling for T-cell activation: relevance to immune responses initiated in skin.
pubmed:affiliation
Department of Dermatology, University of Freiburg, Germany.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Review, Research Support, Non-U.S. Gov't