Linked Life Data

15585889

Source:http://linkedlifedata.com/resource/pubmed/id/15585889

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
2004-12-8
pubmed:abstractText
We previously suggested that CD8(+) T cells promoted resolution of granulomatous experimental autoimmune thyroiditis (G-EAT) at least in part through regulation of Fas ligand (FasL) expression on thyroid epithelial cells. To directly evaluate the role of the Fas pathway in G-EAT resolution, Fas- and FasL-deficient mice on the NOD.H-2h4 background were used as recipients of activated G-EAT effector cells. When MTg-primed wild-type (WT) donor splenocytes were activated and transferred to WT recipients, thyroid lesions reached maximal severity on day 20 and resolved on day 50. Fas, FasL, and FLIP were up-regulated, and many apoptotic inflammatory cells were detected in recipient thyroids on day 20. Fas was predominantly expressed by inflammatory cells, and FasL and FLIP were mainly expressed by thyroid epithelial cells. After depletion of CD8(+) T cells, G-EAT resolution was delayed, FLIP and FasL were predominantly expressed by inflammatory cells, and few inflammatory cells were apoptotic. When WT donor splenocytes were transferred to gld recipients, disease severity on day 20 was similar to that in WT recipients, but resolution was delayed. As in CD8-depleted WT recipients, there were few apoptotic inflammatory cells, and FLIP and FasL were expressed primarily by inflammatory cells. These results indicated that the expression of functional FasL in recipient mice was critical for G-EAT resolution. WT cells induced minimal disease in lpr recipients. This was presumably because donor cells were eliminated by the increased FasL on lpr recipient cells, because donor cells were not eliminated, and the mice developed G-EAT if lpr recipients were given anti-FasL mAb.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
173
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7615-21
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:15585889-Adoptive Transfer, pubmed-meshheading:15585889-Animals, pubmed-meshheading:15585889-Antigens, CD95, pubmed-meshheading:15585889-Apoptosis, pubmed-meshheading:15585889-CASP8 and FADD-Like Apoptosis Regulating Protein, pubmed-meshheading:15585889-Cell Survival, pubmed-meshheading:15585889-Fas Ligand Protein, pubmed-meshheading:15585889-Female, pubmed-meshheading:15585889-Granuloma, pubmed-meshheading:15585889-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:15585889-Ligands, pubmed-meshheading:15585889-Male, pubmed-meshheading:15585889-Membrane Glycoproteins, pubmed-meshheading:15585889-Mice, pubmed-meshheading:15585889-Mice, Inbred MRL lpr, pubmed-meshheading:15585889-Mice, Inbred NOD, pubmed-meshheading:15585889-Mice, Knockout, pubmed-meshheading:15585889-Signal Transduction, pubmed-meshheading:15585889-Spleen, pubmed-meshheading:15585889-Thyroid Gland, pubmed-meshheading:15585889-Thyroiditis, Autoimmune
pubmed:year
2004
pubmed:articleTitle
Fas ligand is required for resolution of granulomatous experimental autoimmune thyroiditis.
pubmed:affiliation
Department of Internal Medicine, University of Missouri School of Medicine, Columbia, MO 65212, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.