Linked Life Data

10946321

Source:http://linkedlifedata.com/resource/pubmed/id/10946321

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2000-9-19
pubmed:abstractText
IL-12 suppresses proallergic Th2-type cytokine production and induces Th1-type cytokine production by peripheral blood T cells from subjects with allergic disease. The objective of the present study was to examine the relevance of these findings to target organ T cell responses in human asthma. Bronchoalveolar lavage (BAL) and PBMC were collected from atopic asthmatics 24 h after fiberoptic allergen challenge of a segmental bronchus. BAL T cells and PBMC were cultured with allergen in the presence of recombinant IL-12 or IFN-gamma, and cytokines were measured in culture supernatants after 6 days. IL-5 production by BAL T cells and PBMC was inhibited by IL-12 and, to a lesser extent, by IFN-gamma. IL-12 also induced IFN-gamma production by BAL T cells and PBMC. The effects of IL-12 nor IFN-gamma on IL-5 production could not be reversed by neutralizing anti-IFN-gamma or anti-IL-12 mAbs, respectively. Thus, the effect of neither IL-12 nor IFN-gamma appeared to be mediated through induction of the other cytokine. In situ hybridization revealed that approximately one-third of BAL T cells expressed mRNA transcripts encoding the IL-12R beta 2 subunit following allergen challenge. Thus, human T cells obtained from BAL during asthmatic late responses, like T cells in the peripheral circulation, remain susceptible to immunomodulation by IL-12. These findings raise the possibility that IL-12 may hold therapeutic potential in allergic diseases such as asthma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
165
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2877-85
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:10946321-Adult, pubmed-meshheading:10946321-Allergens, pubmed-meshheading:10946321-Animals, pubmed-meshheading:10946321-Antibodies, Monoclonal, pubmed-meshheading:10946321-Asthma, pubmed-meshheading:10946321-Bronchoalveolar Lavage Fluid, pubmed-meshheading:10946321-Clone Cells, pubmed-meshheading:10946321-Cytokines, pubmed-meshheading:10946321-Epitopes, T-Lymphocyte, pubmed-meshheading:10946321-Female, pubmed-meshheading:10946321-Humans, pubmed-meshheading:10946321-Interferon-gamma, pubmed-meshheading:10946321-Interleukin-12, pubmed-meshheading:10946321-Interleukin-5, pubmed-meshheading:10946321-Male, pubmed-meshheading:10946321-Mites, pubmed-meshheading:10946321-Pollen, pubmed-meshheading:10946321-RNA, Messenger, pubmed-meshheading:10946321-Receptors, Interleukin, pubmed-meshheading:10946321-Receptors, Interleukin-12, pubmed-meshheading:10946321-T-Lymphocyte Subsets, pubmed-meshheading:10946321-Time Factors
pubmed:year
2000
pubmed:articleTitle
T cells from human allergen-induced late asthmatic responses express IL-12 receptor beta 2 subunit mRNA and respond to IL-12 in vitro.
pubmed:affiliation
Upper Respiratory Medicine, Imperial College School of Medicine at National Heart and Lung Institute, London, United Kingdom.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't