Linked Life Data

9498757

Source:http://linkedlifedata.com/resource/pubmed/id/9498757

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1998-3-18
pubmed:abstractText
Epithelial cells and lymphocytes, including gammadelta and alphabeta T cells, in the gastrointestinal tract epithelium represent a major host defense intranet that is incompletely understood. Cell-to-cell interactions between intraepithelial lymphocytes (IELs) and intestinal epithelial cells (IECs) comprise this intranet, and we have assessed the role of IECs in the regulation of gammadelta and alphabeta T cell responses. When highly purified CD3+ IEL T cells were stimulated via the TCR-CD3 complex, high proliferative responses and cytokine synthesis were induced. However, the addition of viable IECs or purified IEC membranes (mIEC) down-regulated T cell proliferative and cytokine responses. Further, the inhibitory effect of mIEC was not restored by antibodies to TGF-beta, CD1d, E-cadherin, or MHC class I or II. This inhibitory effect was noted for both gammadelta and alphabeta T cell subsets from IELs, and mRNA levels were reduced for both Th1 (IL-2 and IFN-gamma) and Th2 (IL-4 and IL-5) cytokines in gammadelta and alphabeta IELs. In contrast, a purified membrane fraction obtained from thymocytes did not inhibit IEL proliferative responses. Further, mIEC did not inhibit splenic alphabeta T cell proliferative responses. These findings show that cell-to-cell interactions between intraepithelial gammadelta and alphabeta T cells and IECs occur via cell surface molecules, suggesting an intranet to prevent potential inflammatory responses at the intestinal mucosal surface.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
160
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2188-96
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:9498757-Animals, pubmed-meshheading:9498757-Antibodies, Blocking, pubmed-meshheading:9498757-Antibodies, Monoclonal, pubmed-meshheading:9498757-Antigens, CD1, pubmed-meshheading:9498757-Cadherins, pubmed-meshheading:9498757-Cell Communication, pubmed-meshheading:9498757-Cell Membrane, pubmed-meshheading:9498757-Cytokines, pubmed-meshheading:9498757-Down-Regulation, pubmed-meshheading:9498757-Epithelial Cells, pubmed-meshheading:9498757-Histocompatibility Antigens Class I, pubmed-meshheading:9498757-Histocompatibility Antigens Class II, pubmed-meshheading:9498757-Intestinal Mucosa, pubmed-meshheading:9498757-Lymphocyte Activation, pubmed-meshheading:9498757-Mice, pubmed-meshheading:9498757-Mice, Inbred C3H, pubmed-meshheading:9498757-Signal Transduction, pubmed-meshheading:9498757-T-Lymphocyte Subsets, pubmed-meshheading:9498757-Transforming Growth Factor beta
pubmed:year
1998
pubmed:articleTitle
A mucosal intranet: intestinal epithelial cells down-regulate intraepithelial, but not peripheral, T lymphocytes.
pubmed:affiliation
Immunobiology Vaccine Center, Department of Oral Biology, University of Alabama Medical Center, Birmingham 35294, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't