Linked Life Data

2525110

Source:http://linkedlifedata.com/resource/pubmed/id/2525110

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1989-7-17
pubmed:abstractText
This paper describes the characteristics of T suppressor inducer (Ts ind) cells which can interact with T suppressor effector (Ts eff) cells and thereby can account for suppression of delayed-type hypersensitivity (DTH) to alloantigens. Adoptive transfer of spleen cells from mice intravenously (i.v.) injected with allogeneic spleen cells one day earlier induced an antigen-specific state of suppression in the recipients. This became apparent when DTH was induced by subcutaneous (s.c.) immunization of the recipients three days after transfer. The induction of suppression after adoptive transfer of spleen cells required Thy-1+, L3T4+, Lyt-1+2- cells. These cells that by themselves did not exert a suppressive effect induced a state of suppression in recipient mice by activation of recipient-type Ts eff cells. Therefore, the former cell type was classified as Ts ind cell. When athymic nude mice were used as recipients, Lyt-2+ precursors of Ts eff cells had to be transferred together with the Ts ind cells to induce a state of suppression in these mice. The Ts ind cells could activate Ts eff cells in MHC- and Igh-incompatible recipients. The results are discussed in relation to previously described immunoregulatory T cell pathways.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0171-2985
pubmed:author
pubmed:issnType
Print
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
56-67
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1989
pubmed:articleTitle
MHC- and Igh-unrestricted interaction between L3T4+, Lyt-2- Ts inducer cells and L3T4-, Lyt-2+ Ts effector cells is required for T cell-dependent suppression of DTH to histocompatibility antigens.
pubmed:affiliation
Department of Cell Biology, Immunology and Genetics, Erasmus University, Rotterdam, The Netherlands.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't