Linked Life Data

7536768

Source:http://linkedlifedata.com/resource/pubmed/id/7536768

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
1995-5-24
pubmed:abstractText
Exposure of naive CD4+ T lymphocytes to superantigens such as staphylococcal enterotoxin B (SEB) induces a strong proliferative response. Prolonged exposure or subsequent restimulation of the responding T cell population with SEB leads to the apoptotic events of activation-induced cell death (AICD). However, T cells derived from either Fas-deficient lpr or Fas ligand-deficient gld autoimmune mouse strains, fail to undergo AICD under these conditions. Instead, these autoimmune T cells mount a vigorous proliferative response, suggesting a critical role for Fas/FasL interactions in this form of autoapoptosis. In the current study, we found that SEB-induced AICD was tied to the rapid induction of FasL expression in cells constitutively expressing high levels of Fas. Furthermore, the addition of soluble Fas-IgG fusion protein to the SEB-restimulated cultures blocked AICD and resulted in a 2 degrees proliferative response that was comparable in magnitude and kinetics to that of the lpr and gld T cells. The rapid onset of apoptosis in normal T cells subsequent to restimulation with SEB was in direct contrast to the proliferative response of the initial cultures, even though comparable levels of Fas and FasL RNA were found in T cells after 1 degree and 2 degrees challenge. The clonal expansion of the normal T cells responding to the initial SEB stimulation was, however, dramatically compromised when the normal cells were cocultured with an MRL-lpr responder population; addition of soluble Fas-IgG rescued the normal component of the response. Together, these data demonstrate first, that Fas/FasL interactions are intimately tied to superantigen-induced AICD, a form of autocrine cell death, and second, that FasL-mediated cytotoxicity is responsible for the disappearance of normal CD4+ T cells in lpr cocultures.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
154
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4302-8
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:7536768-Animals, pubmed-meshheading:7536768-Antigens, CD3, pubmed-meshheading:7536768-Antigens, CD95, pubmed-meshheading:7536768-Antigens, Surface, pubmed-meshheading:7536768-Apoptosis, pubmed-meshheading:7536768-Base Sequence, pubmed-meshheading:7536768-CD4-Positive T-Lymphocytes, pubmed-meshheading:7536768-Cells, Cultured, pubmed-meshheading:7536768-Cytotoxicity, Immunologic, pubmed-meshheading:7536768-Enterotoxins, pubmed-meshheading:7536768-Fas Ligand Protein, pubmed-meshheading:7536768-Flow Cytometry, pubmed-meshheading:7536768-Immunoglobulin G, pubmed-meshheading:7536768-Membrane Glycoproteins, pubmed-meshheading:7536768-Mice, pubmed-meshheading:7536768-Mice, Mutant Strains, pubmed-meshheading:7536768-Molecular Sequence Data, pubmed-meshheading:7536768-Recombinant Fusion Proteins, pubmed-meshheading:7536768-Superantigens, pubmed-meshheading:7536768-Up-Regulation
pubmed:year
1995
pubmed:articleTitle
Fas ligand-mediated cytotoxicity is directly responsible for apoptosis of normal CD4+ T cells responding to a bacterial superantigen.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, Boston University School of Medicine, MA 02118, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't