Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
3
|
| pubmed:dateCreated |
1999-4-13
|
| pubmed:abstractText |
Autocrine interaction of Fas and Fas ligand leads to apoptosis of activated T cells, a process that is critical for the maintenance of peripheral T cell tolerance. Paracrine interactions of Fas ligand with T cells also may play an important role in the maintenance of tolerance, as Fas ligand can create immune-privileged sites and prevent graft rejection by inducing apoptosis in T cells. We surmised that APCs that express Fas ligand might directly induce apoptosis of T cells during presentation of Ag to the T cells, thus inducing Ag-specific, systemic T cell tolerance. Here, we show that profound, specific T cell unresponsiveness to alloantigen was induced by treatment of H-2k mice with H-2b APCs that expressed Fas ligand and that profound T cell unresponsiveness specific for the H-Y Ag was induced by treatment of H-2Db/H-Y TCR transgenic female mice with H-2Db/H-Y APCs that expressed Fas ligand. The induction of this systemic T cell tolerance required the expression of Fas ligand on the APCs as well as the expression of Fas on the T cells. The tolerance was restricted to the Ag presented by the APCs. The rapid and profound clonal deletion of the Ag-specific, peripheral T cells mediated by the Fas ligand-expressing APCs contributed to the induction of tolerance. These findings demonstrate that Ag-specific T cell tolerance can be induced by APCs that express Fas ligand and suggest a novel function for APCs in the induction of T cell apoptosis. Furthermore, they indicate a novel immunointervention strategy for treatment of graft rejection and autoantigen-specific autoimmune diseases.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
AIM
|
| pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD95,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Fasl protein, mouse,
http://linkedlifedata.com/resource/pubmed/chemical/H-2 Antigens,
http://linkedlifedata.com/resource/pubmed/chemical/H-Y Antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Isoantigens,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell
|
| pubmed:status |
MEDLINE
|
| pubmed:month |
Feb
|
| pubmed:issn |
0022-1767
|
| pubmed:author | |
| pubmed:issnType |
Print
|
| pubmed:day |
1
|
| pubmed:volume |
162
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
1423-30
|
| pubmed:dateRevised |
2007-11-14
|
| pubmed:meshHeading |
pubmed-meshheading:9973398-Animals,
pubmed-meshheading:9973398-Antigen-Presenting Cells,
pubmed-meshheading:9973398-Antigens, CD95,
pubmed-meshheading:9973398-Apoptosis,
pubmed-meshheading:9973398-Fas Ligand Protein,
pubmed-meshheading:9973398-Female,
pubmed-meshheading:9973398-H-2 Antigens,
pubmed-meshheading:9973398-H-Y Antigen,
pubmed-meshheading:9973398-Immune Tolerance,
pubmed-meshheading:9973398-Isoantigens,
pubmed-meshheading:9973398-Lymphoid Tissue,
pubmed-meshheading:9973398-Macrophages,
pubmed-meshheading:9973398-Male,
pubmed-meshheading:9973398-Membrane Glycoproteins,
pubmed-meshheading:9973398-Mice,
pubmed-meshheading:9973398-Mice, Inbred C57BL,
pubmed-meshheading:9973398-Mice, Inbred MRL lpr,
pubmed-meshheading:9973398-Mice, Transgenic,
pubmed-meshheading:9973398-Receptors, Antigen, T-Cell,
pubmed-meshheading:9973398-T-Lymphocytes
|
| pubmed:year |
1999
|
| pubmed:articleTitle |
Induction of specific T cell tolerance by Fas ligand-expressing antigen-presenting cells.
|
| pubmed:affiliation |
Division of Clinical Immunology and Rheumatology, University of Alabama, Birmingham, AL 35294, USA.
|
| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|