Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1995-12-14
pubmed:abstractText
NK-like cytotoxicity in F1-hybrid mice with acute GVH disease is mediated by donor-derived CD3+/CD4-/CD8- cells that can lyse both NK-sensitive YAC-1 target cells as well as NK-resistant targets such as BW1100 and P815. Our objective was to determine whether this activity is mediated by gamma delta TCR+ cells. We showed that NK-like cytotoxic activity in the spleen and lymph nodes of mice with acute GVH disease could be depleted by indirect complement-mediated lysis using an Ab against gamma delta TCR. When purified NK1.1+ spleen cells that had been positively selected on a magnetic cell separator were used as effector cells, we found that NK-like cytotoxicity was mediated only by gamma delta TCR+ cells, suggesting that cells with NK-like activity are gamma delta TCR+/NK1.1+. We showed by flow cytometry experiments that coexpression of NK1.1 and TCR-gamma delta occurred on a large proportion of large granular lymphocytes in the spleens of GVH mice, but was not detectable in normal control mice. In GVH mice, fewer than 10% of small agranular NK1.1+ lymphocytes coexpressed NK1.1+ and gamma delta TCR+. On the basis of this hypothesis, we postulate that graft-derived large granular lymphocytes develop the NK1.1+/gamma delta TCR+ phenotype during the reaction, and that these cells play a role in the pathogenesis of acute GVH disease. We performed experiments to determine whether depletion of gamma delta T cells from donor mice affected the outcome of lethal GVH disease and found that there was a significant reduction in mortality.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
155
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4189-98
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:7594574-Acute Disease, pubmed-meshheading:7594574-Animals, pubmed-meshheading:7594574-Antigens, pubmed-meshheading:7594574-Antigens, Ly, pubmed-meshheading:7594574-Antigens, Surface, pubmed-meshheading:7594574-Cytotoxicity, Immunologic, pubmed-meshheading:7594574-Female, pubmed-meshheading:7594574-Flow Cytometry, pubmed-meshheading:7594574-Graft vs Host Disease, pubmed-meshheading:7594574-Immunophenotyping, pubmed-meshheading:7594574-Killer Cells, Natural, pubmed-meshheading:7594574-Lectins, C-Type, pubmed-meshheading:7594574-Lymph Nodes, pubmed-meshheading:7594574-Mice, pubmed-meshheading:7594574-Mice, Inbred BALB C, pubmed-meshheading:7594574-Mice, Inbred C3H, pubmed-meshheading:7594574-Mice, Inbred C57BL, pubmed-meshheading:7594574-Mice, Inbred DBA, pubmed-meshheading:7594574-NK Cell Lectin-Like Receptor Subfamily B, pubmed-meshheading:7594574-Proteins, pubmed-meshheading:7594574-Receptors, Antigen, T-Cell, gamma-delta, pubmed-meshheading:7594574-Spleen, pubmed-meshheading:7594574-T-Lymphocytes, Cytotoxic, pubmed-meshheading:7594574-Weight Loss
pubmed:year
1995
pubmed:articleTitle
Gamma delta T cells in the pathobiology of murine acute graft-versus-host disease. Evidence that gamma delta T cells mediate natural killer-like cytotoxicity in the host and that elimination of these cells from donors significantly reduces mortality.
pubmed:affiliation
Department of Immunology, University of Manitoba, Winnipeg, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't