Linked Life Data

6242856

Source:http://linkedlifedata.com/resource/pubmed/id/6242856

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1989-8-21
pubmed:abstractText
The generation of functionally active immunoregulatory T lymphocytes has been shown to depend upon the interaction of a number of different immune cell types during development. In order to understand and perhaps manipulate immunoregulatory T cell interactions, it is important to identify the nature and role of these cell types in the immunoregulatory T cell pathway. We have investigated the role of Ig+ B cells in the generation of suppressor T lymphocytes in the immune response to SRBC. Our approach was to suppress the expression of Ig+ B cells in experimental mice by continuously treating these animals with a rabbit anti-mu-chain antiserum. These animals were simultaneously tested for their ability to make suppressor T cell responses as measured by the ability to produce or accept SRBC-specific suppressor T cell factors. This particular approach, neonatal suppression with anti-mu-chain antibody, has been previously shown to be an effective means of depleting animals of Ig+ cells, while having little or no effect on a number of different T cell-mediated responses, including T cell mediated allograft rejection and delayed-type hypersensitivity responses in vivo as well as the generation of MLR and CTL responses to alloantigens and conventional I-A recognizing T helper cell responses in vitro. Our results indicate that anti-mu-treated mice lack the ability to produce both Ly1 and Ly2 cell-derived suppressor factors when immunized with the relevant antigen SRBC. Further, while the T cells from anti-mu-treated mice were capable of generating a T helper cell response to SRBC in vitro, these T cells no longer responded to suppressor cell signals from either the Ly1 or Ly2 T cell-derived suppressor factors. The ability to produce or accept suppressor cell signals was traced to the lack of an I-J+ Ly1 T cell absent in anti-mu-treated mice. This cell produces an I-J+ antigen nonspecific molecule which imparts Igh-V linked genetic restrictions to both the Ly1 and Ly2 T cell derived suppressor factors. The results alter our view on immune regulation by suggesting that both the induction and effector phase of suppressor T cell activity to SRBC is dependent upon an antigen nonspecific Ly1 I-J+ T cell which is distinct from the antigen recognizing I-J- T cells required for antigen-specific suppression. This I-J+ T cell, which imparts an Igh-linked restriction to the suppressor factors, is critically dependent on Ig+ B cells to reach a functionally active state.(ABSTRACT TRUNCATED AT 400 WORDS)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0724-6803
pubmed:author
pubmed:issnType
Print
pubmed:volume
1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
167-76
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1984
pubmed:articleTitle
B cell-deprived mice lack functional expression of certain T suppressor cell subsets.
pubmed:affiliation
Department of Pathology, Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, Connecticut 06510.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't