Linked Life Data

7677228

Source:http://linkedlifedata.com/resource/pubmed/id/7677228

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
25 Suppl
pubmed:dateCreated
1995-10-19
pubmed:abstractText
An animal model system was developed to study the mechanisms resulting in allergic sensitization. Local allergen exposure via the airways and the lung stimulated an allergen-specific immunoglobulin E (IgE) response that was paralleled by the development of increased airway responsiveness (AR). It was found that CD4+ T cells of local draining lymph nodes played an important role in the regulation of these events. Stimulation of allergen-specific T cells requires interaction between major histocompatibility complex (MHC) class II molecules (expressed on antigen-presenting cells), peptide (presented on MHC) and the T cell receptor. Allergen sensitization stimulated T cells that expressed a restricted T cell receptor V beta (TCR-V beta) elements. Each allergen stimulated different V beta elements, and sensitization to the same allergen resulted in a different pattern of TCR-V beta stimulation in different lymphoid tissues. Some of these T cells had pro-allergenic effects, whereas others were able to inhibit the development of the allergic response, including the development of increased AR. These data indicate that the local T cell response regulates the type of immune response that evolves following local allergen sensitization.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0105-4538
pubmed:author
pubmed:issnType
Print
pubmed:volume
50
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
15-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1995
pubmed:articleTitle
T cell receptor-V beta repertoire in allergen-specific sensitization and increased airway responsiveness.
pubmed:affiliation
Institut für Klinische Chemie und Biochemie, Freie Universität Berlin, Germany.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't