Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1996-7-16
pubmed:abstractText
T cells with antidonor specificities have been isolated from human recipients experiencing graft rejection after allogeneic bone marrow transplantation (BMT). Partial T-cell depletion of unrelated BM grafts with an anti- T-cell receptor (TCR) monoclonal antibody (MoAb) directed against the TCR alpha/beta heterodimer have shown that the incidence of graft-versus-host disease is low and that the incidence of durable engraftment is high. These studies suggest either that the number of residual TCR alpha/beta+ cells was sufficient to permit alloengraftment or that the preservation of cells other than TCR alpha/beta+ cells was beneficial for engraftment. With respect to the latter, one such candidate cell is the TCR gamma/delta+ T cell. Because no studies have specifically examined whether TCR gamma/delta+ cells might be capable of eliminating BM-derived hematopoietic cells, we established a new graft rejection model system in which transgenic (Tg) H-2d mice (termed G8), known to express gamma/delta heterodimers on high proportion of peripheral T cells, were used as BMT recipients. These Tg TCR gamma/delta+ cells respond vigorously to target cells that express the nonclassical major histocompatibility complex (MHC) class lb region gene products encoded in H-2T region of H-2T(b)+ strains. G8 Tg mice were used as recipients for C57BL/6 (B6: H-2(b); H-2T(b)) T-cell-depleted (TCD) donor BM. We show that G8 Tg (H-2(d), H-2T(d)) mice are potent mediators of B6 BM graft rejection and that the rejection process was inhibited by anti-TCR gamma/delta MoAbs. In contrast, BM from a B6 congenic strain that expresses the H-2T(a) allele, B6.A-Tl(a)/BoyEg, was readily accepted, suggesting that H-2T antigens on repopulating donor BM cells are the targets of host graft rejecting T cells that express the TCR gamma/delta heterodimer. PB chimerism studies were performed at > or = 1.5 months post-BMT using TCD BM from severe combined immunodeficient allogeneic donors, which is highly susceptible to rejection by the host. The addition of donor G8 TCR gamma/delta+ cells to TCD donor BM was shown to significantly increase alloengraftment in B6 recipients. These results show that (1) host TCR gamma/delta+ cells can reject repopulating donor cells, presumably by responding to nonclassical MHC class lb gene products expressed on BM-derived hematopoietic progenitor cells; and (2) donor TCR gamma/delta+ cells can facilitate the alloengraftment of rigorously TCD donor BM.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
87
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4463-72
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:8639809-Animals, pubmed-meshheading:8639809-Antibodies, Monoclonal, pubmed-meshheading:8639809-Antigens, CD3, pubmed-meshheading:8639809-Bone Marrow Transplantation, pubmed-meshheading:8639809-Female, pubmed-meshheading:8639809-G(M1) Ganglioside, pubmed-meshheading:8639809-Graft Rejection, pubmed-meshheading:8639809-H-2 Antigens, pubmed-meshheading:8639809-Histocompatibility Antigens Class I, pubmed-meshheading:8639809-Lymphocyte Activation, pubmed-meshheading:8639809-Male, pubmed-meshheading:8639809-Mice, pubmed-meshheading:8639809-Mice, Inbred BALB C, pubmed-meshheading:8639809-Mice, Inbred C57BL, pubmed-meshheading:8639809-Mice, SCID, pubmed-meshheading:8639809-Mice, Transgenic, pubmed-meshheading:8639809-Radiation Chimera, pubmed-meshheading:8639809-Receptors, Antigen, T-Cell, gamma-delta, pubmed-meshheading:8639809-Severe Combined Immunodeficiency, pubmed-meshheading:8639809-T-Lymphocyte Subsets, pubmed-meshheading:8639809-Transplantation, Homologous
pubmed:year
1996
pubmed:articleTitle
Murine gamma/delta-expressing T cells affect alloengraftment via the recognition of nonclassical major histocompatibility complex class Ib antigens.
pubmed:affiliation
Department of Pediatrics, University of Minnesota Hospital, Minneapolis, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't