Linked Life Data

3895538

Source:http://linkedlifedata.com/resource/pubmed/id/3895538

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1985-9-6
pubmed:abstractText
The interdependence between immunologic events occurring within acutely rejecting rat cardiac allografts and those in host lymphoid tissues were studied. To evaluate cellular dynamics of allograft infiltration, 111In-labeled thoracic duct lymphocytes from Lewis rats were administered intravenously daily (0 to 7 days after transplantation) to (Lewis X BN)F1 heart-grafted unmodified Lewis rats, sacrificed 24 hours later. Accumulation of thoracic duct lymphocytes in the allografts peaked 4 to 5 days after transplantation. To evaluate whether these changes at the graft site were sufficient to carry on the rejection response in the absence of a sustained host immunologic drive, acutely rejecting (Lewis X BN)F1 cardiac allografts were retransplanted serially at days 1 through 5 into normal syngeneic animals. All these regrafts survived greater than 100 days. Neither infusion of interleukin-2-conditioned medium (100 IU for 7 days intravenously) into regrafted hosts nor preoperative perfusion of the retransplanted hearts with interleukin-2-conditioned medium (300 IU) could complete the rejection process. Using flow cytometry analysis, we then assessed the phenotypic alterations of the mononuclear cells infiltrating the graft. The ratio of T helper: T cytotoxic/suppressor cells, which at day 3 was 1.57, inverted abruptly to 0.67 by days 5 to 6. After retransplantation a dramatic depression in T-lymphocyte subsets occurred, particularly affecting the T cytotoxic/suppressor phenotype. Trafficking studies revealed that the T cells that left the regrafts migrated mainly to spleen and mesenteric lymph nodes and away from bone marrow and peripheral blood of the syngeneic secondary recipients. Finally, histologic manifestations of acute rejection at days 4 to 5 virtually reversed themselves after regrafting. These studies emphasize the systemic nature of the rejection cascade, which depends fully on the host lymphoid system; even late changes in the graft microenvironment are not sufficient to produce final immunologic destruction.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0039-6060
pubmed:author
pubmed:issnType
Print
pubmed:volume
98
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
259-66
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1985
pubmed:articleTitle
Host-graft relationship: the systemic nature of allograft rejection.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.