Linked Life Data

16177624

Source:http://linkedlifedata.com/resource/pubmed/id/16177624

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2005-9-22
pubmed:abstractText
A key factor driving the underlying pathyphysiology of "chronic rejection" in organ transplantation is a persistent T cell-mediated alloimmune response. Members of both the B7 family (including CD28 and CTLA4) and the tumor necrosis factor (TNF) family, in which the CD40-CD154 pathway is preeminent, play key roles in the T cell response following alloantigen presentation. "Positive" costimulatory molecules promote full T cell activation, whereas a subgroup of costimulatory molecules delivers "negative" costimulatory signals that function to downregulate alloimmune responses. Emerging experimental data point to key differences between the various positive and negative costimulatory molecules in terms of their temporal and spatial expression profiles, their effects of T and B cell subsets, and on their relative importance within the hierarchy of costimulatory signals delivered to the T cell. In this review, we address the role of costimulatory pathways in allograft rejection and tolerance. We will address in particular the potential of the novel costimulatory pathways as targets for tolerance induction in CD28-independent alloresponses, and we will review emerging data that suggests a key role for parenchymal expression of negative costimulatory molecules in the termination of pathogenic immune responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0041-1337
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
80
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
555-63
pubmed:meshHeading
pubmed:year
2005
pubmed:articleTitle
T-cell costimulatory pathways in allograft rejection and tolerance.
pubmed:affiliation
Transplantation Research Center, Brigham and Women's Hospital and Children's Hospital Boston, Harvard Medical School, Boston, MA, USA. mrclarkson@partners.org
pubmed:publicationType
Journal Article, Review