Linked Life Data

17181648

Source:http://linkedlifedata.com/resource/pubmed/id/17181648

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2006-12-21
pubmed:abstractText
In order to prevent allograft rejection, most current immunosuppressive drugs nonspecifically target T-cell activation, clonal expansion or differentiation into effector cells. Experimental models have shown that it is possible to exploit the central and peripheral mechanisms that normally maintain immune homeostasis and tolerance to self-antigens, in order to induce tolerance to alloantigens. Central tolerance results from intrathymic deletion of T cells with high avidity for thymically expressed antigens. Peripheral tolerance to nonself-molecules can be achieved by various mechanisms including deletion of activated/effector T cells, anergy induction and active regulation of effector T cells. In this article, we briefly discuss the pathways of allorecognition and their relevance to current immunosuppressive strategies and to the induction of transplantation tolerance (through haematopoietic mixed chimerism, depleting protocols, costimulatory blockade and regulatory T cells). We then review the prospect of clinical applicability of these protocols in solid organ transplantation.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0934-0874
pubmed:author
pubmed:issnType
Print
pubmed:volume
20
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
12-24
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
From current immunosuppressive strategies to clinical tolerance of allografts.
pubmed:affiliation
Transplantation Centre and Transplantation Immunopathology Laboratory, University Hospital Lausanne, Lausanne, Switzerland. dela.golshayan@chuv.ch
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't