Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1994-8-16
pubmed:abstractText
Spontaneous orthotopic liver allograft acceptance associated with microchimerism in mice induces tolerance to subsequent skin or heart transplants from the donor but not third-party animals. Despite in vivo hyporesponsiveness, in vitro MLC and CTL assays showed continuing antidonor reactivity. Cells isolated from recipients' spleens and grafted livers, when tested in MLC and CTL assays, were antidonor reactive out to 3 months to the same degree as splenocytes obtained from either naive or presensitized (with skin or heart) mice. Nevertheless, passive transfer of splenocytes or liver lymphocytes from liver tolerant mice, but not naive or sensitized donor strain mice, were able to prolong skin graft survival significantly in naive irradiated recipients. By using a strain combination in which the donor but not the recipient expressed the stimulatory endogenous super-Ag (Mlsf), it was possible to determine whether super-Ag-reactive T cells bearing V beta 5 and V beta 11 were deleted or anergic. Phenotypic analysis of cells isolated from recipients' spleens and grafted livers (up to 90 days after transplant), when compared with naive animals, showed no significant difference in V beta 5 and V beta 11 TCR expression. Additionally, when these isolated spleen cells were tested for antibody-mediated stimulation, both anti-V beta 5 and V beta 11 TCR mAb led to marked proliferation of cells obtained from naive and liver-transplanted recipients, but as expected, proliferation was very low in cells from naive donors. These results suggest that liver transplantation induces donor-specific tolerance in vivo, which may not be reflected in in vitro proliferative and cytotoxicity assays (split tolerance). Furthermore, this tolerance does not seem to be induced by clonal deletion or anergy of minor-lymphocyte-stimulating-antigen-reactive T cells in the recipients.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0041-1337
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1-8
pubmed:dateRevised
2011-11-4
pubmed:meshHeading
pubmed-meshheading:8036695-Animals, pubmed-meshheading:8036695-Cytotoxicity, Immunologic, pubmed-meshheading:8036695-Graft Survival, pubmed-meshheading:8036695-Immune Tolerance, pubmed-meshheading:8036695-Immunotherapy, Adoptive, pubmed-meshheading:8036695-Liver Transplantation, pubmed-meshheading:8036695-Lymphocyte Activation, pubmed-meshheading:8036695-Male, pubmed-meshheading:8036695-Mice, pubmed-meshheading:8036695-Mice, Inbred BALB C, pubmed-meshheading:8036695-Mice, Inbred C3H, pubmed-meshheading:8036695-Mice, Inbred C57BL, pubmed-meshheading:8036695-Minor Lymphocyte Stimulatory Antigens, pubmed-meshheading:8036695-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:8036695-Skin Transplantation, pubmed-meshheading:8036695-Spleen, pubmed-meshheading:8036695-T-Lymphocytes, pubmed-meshheading:8036695-Transplantation, Homologous
pubmed:year
1994
pubmed:articleTitle
Split tolerance induced by orthotopic liver transplantation in mice.
pubmed:affiliation
Pittsburgh Transplant Institute, University of Pittsburgh Medical Center, Pennsylvania 15213.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't