Linked Life Data

16272282

Source:http://linkedlifedata.com/resource/pubmed/id/16272282

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2005-11-7
pubmed:abstractText
Chemokine receptor blockade can diminish the recruitment of host effector cells and prolong allograft survival, but little is known of the role of chemokine receptors in promoting host sensitization. We engrafted fully allogeneic islets into streptozotocin-treated normal mice or mice with the autosomal recessive paucity of lymph node T cell (plt) mutation; the latter lack secondary lymphoid expression of the CCR7 ligands, secondary lymphoid organ chemokine (CCL21) and EBV-induced molecule-1 ligand chemokine (CCL19). plt mice showed permanent survival of islets engrafted under the kidney capsule, whereas controls rejected islet allografts in 12 days (p < 0.001), and consistent with this, plt mice had normal allogeneic T cell responses, but deficient migration of donor dendritic cell to draining lymph nodes. Peritransplant i.v. injection of donor splenocytes caused plt recipients to reject their allografts by 12 days, and sensitization at 60 days posttransplant of plt mice with well-functioning allografts restored acute rejection. Finally, islet allografts transplanted intrahepatically in plt mice were rejected approximately 12 days posttransplant, like controls, as were primarily revascularized cardiac allografts. These data show that the chemokine-directed homing of donor dendritic cell to secondary lymphoid tissues is essential for host sensitization and allograft rejection. Interruption of such homing can prevent T cell priming and islet allograft rejection despite normal T and B cell functions of the recipient, with potential clinical implications.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
175
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6311-8
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:16272282-Animals, pubmed-meshheading:16272282-B-Lymphocytes, pubmed-meshheading:16272282-Chemokine CCL19, pubmed-meshheading:16272282-Chemokine CCL21, pubmed-meshheading:16272282-Chemokines, CC, pubmed-meshheading:16272282-Dendritic Cells, pubmed-meshheading:16272282-Graft Rejection, pubmed-meshheading:16272282-Graft Survival, pubmed-meshheading:16272282-Heart Transplantation, pubmed-meshheading:16272282-Islets of Langerhans Transplantation, pubmed-meshheading:16272282-Lymph Nodes, pubmed-meshheading:16272282-Lymphocyte Activation, pubmed-meshheading:16272282-Major Histocompatibility Complex, pubmed-meshheading:16272282-Mice, pubmed-meshheading:16272282-Mice, Inbred BALB C, pubmed-meshheading:16272282-Mice, Inbred C57BL, pubmed-meshheading:16272282-Mice, Inbred DBA, pubmed-meshheading:16272282-Mice, Mutant Strains, pubmed-meshheading:16272282-Receptors, CCR7, pubmed-meshheading:16272282-Receptors, Chemokine, pubmed-meshheading:16272282-T-Lymphocytes, pubmed-meshheading:16272282-Transplantation, Homologous
pubmed:year
2005
pubmed:articleTitle
Permanent survival of fully MHC-mismatched islet allografts by targeting a single chemokine receptor pathway.
pubmed:affiliation
Division of Transplantation Immunology, Department of Pathology and Laboratory Medicine, Joseph Stokes Jr. Research Institute and Biesecker Pediatric Liver Center, Philadelphia, PA 19104, USA.
pubmed:publicationType
Journal Article