Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1994-12-28
pubmed:abstractText
Transfer of a certain number of C57BL/6 (B6) spleen cells into (BALB/cxB6)F1 (CB6F1) nu/nu mice, which are deficient in T cells, causes lethal graft-versus-host disease (GVHD) in the recipients. However, when normal CB6F1 mice are used as recipients, lethal GVHD does not occur. Using this lethal GVHD system, we investigated which roles CD4+ and CD8+ T cells play in the resistance to lethal GVHD induction by parent cell transfer in the normal F1 hybrid host. Lethal GVHD induction by B6 spleen cells in CB6F1 nu/nu mice was blocked by prior reconstitution of the recipients with normal syngeneic spleen cells. In addition, all nu/nu mice reconstituted with syngeneic CD8+ spleen cells developed lethal GVHD, whereas none of the nu/nu mice reconstituted with CD4+ cells did. Both spleen weight and number of spleen cells in the former prominently decreased in contrast to the slight increase (peak at 15 weeks) seen in the latter after transfer of donor spleen cells. H-2Dd- Thy1.2+ cells, which are considered to derive from donor B6 T cells, existed in the spleen from the CD4+ spleen cell-reconstituted GVHD mice, peaking at 5 weeks then gradually decreasing after transfer of donor cells. However, they disappeared in the normal spleen cell-reconstituted GVHD mice 5 weeks later. These findings suggest that CD4+ cells in the normal F1 hybrid host play a critical role in the resistance to lethal GVHD induction by parent spleen cell transfer, although CD8+ cells are required for the prompt elimination of donor cells.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0165-2478
pubmed:author
pubmed:issnType
Print
pubmed:volume
40
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
207-10
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
The role of CD4+ and CD8+ cells in normal F1 hybrid host in the resistance to lethal graft-versus-host disease induction by transfer of parent spleen cells.
pubmed:affiliation
Department of Dermatology, Faculty of Medicine, Kyoto University, Japan.
pubmed:publicationType
Journal Article