Linked Life Data

15905589

Source:http://linkedlifedata.com/resource/pubmed/id/15905589

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
2005-5-20
pubmed:abstractText
Immune coagulation is a major contributor to the pathogenesis of xenograft rejection, viral-induced hepatocellular injury and cytokine-induced fetal loss syndrome. In this study, we investigated the contribution of the novel gene product, fibrinogen-like protein 2 (fgl2) prothrombinase, in mediating immune injury in experimental and human acute allograft rejection. Using a mouse heterotopic cardiac transplant model, mouse fgl2(mfgl2)/fibroleukin mRNA transcripts and protein were highly expressed in macrophages, CD4- and CD8-positive T lymphocytes, and endothelial cells in rejecting cardiac allografts in association with deposits of fibrin. Although mfgl2-deficient mice rejected allografts at similar rates to littermate controls, survival of grafts from mfgl2-deficient mice were prolonged and deposition of intravascular fibrin was diminished. Treatment of wild-type mice with a neutralizing anti-fgl2 Ab ameliorated histological evidence for allorejection and intravascular fibrin deposition, and resulted in an increase in graft survival. To address further the relevance of fgl2 in acute allograft rejection, we examined kidney biopsies from patients who had undergone renal transplantation. Human fgl2 mRNA transcripts and protein were markedly expressed mainly in renal tubule cells, infiltrating lymphoid cells including macrophages, CD8(+) T cells, mature B cells (plasma cells), and endothelial cells. Dual staining showed fibrin deposition was localized mainly to blood vessels, in the glomerulus and interstitium and the lumen of tubules, and occurred in association with human fgl2 expression. These data collectively suggest that fgl2 accounts for the fibrin deposition seen in both experimental and human allograft rejection and provide a rationale for targeting fgl2 as adjunctive therapy to treat allograft rejection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
174
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
7403-11
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:15905589-Adult, pubmed-meshheading:15905589-Animals, pubmed-meshheading:15905589-Female, pubmed-meshheading:15905589-Fibrin, pubmed-meshheading:15905589-Fibrinogen, pubmed-meshheading:15905589-Graft Rejection, pubmed-meshheading:15905589-Graft Survival, pubmed-meshheading:15905589-Heart Transplantation, pubmed-meshheading:15905589-Humans, pubmed-meshheading:15905589-Immune Sera, pubmed-meshheading:15905589-Immunohistochemistry, pubmed-meshheading:15905589-Kidney Transplantation, pubmed-meshheading:15905589-Male, pubmed-meshheading:15905589-Mice, pubmed-meshheading:15905589-Mice, Inbred BALB C, pubmed-meshheading:15905589-Mice, Inbred C57BL, pubmed-meshheading:15905589-Mice, Knockout, pubmed-meshheading:15905589-Middle Aged, pubmed-meshheading:15905589-Thromboplastin, pubmed-meshheading:15905589-Transplantation, Heterotopic, pubmed-meshheading:15905589-Transplantation, Homologous
pubmed:year
2005
pubmed:articleTitle
Role of fibrinogen-like protein 2 prothrombinase/fibroleukin in experimental and human allograft rejection.
pubmed:affiliation
Laboratory of Infectious Immunology, Department of Infectious Disease, Institute of Immunology, Huazhong University of Science and Technology, Wuhan, China. qning@tjh.tjmu.edu.cn
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't