Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1998-4-20
pubmed:abstractText
Cross-linking of cell surface CD4 molecules by anti-CD4 mAb or HIV-1 gp120/anti-gp120 Ab primes resting T lymphocytes for activation-induced cell death (AICD) triggered via the CD3/TCR complex. In striking contrast, we demonstrate here that preincubation of activated human CD4+ T cells with anti-CD4 mAb consistently inhibited AICD triggered via anti-CD3 mAb or Staphylococcus aureus enterotoxin A superantigen. Inhibition of AICD of CD4+ T cell clones was also observed with F(ab')2, but not with Fab, of anti-CD4 mAb. Moreover, soluble HIV-1 gp120, but not rIL-16, inhibited AICD stimulated by S. aureus enterotoxin A. In susceptible clones, CD4 ligation prevented the up-regulation of Fas ligand mRNA and cell surface expression in response to anti-CD3 mAb or superantigen stimulation. CD3/TCR-dependent protein tyrosine phosphorylation and cytokine production were also prevented by preceding CD4 ligation. The inhibition of AICD due to the prevention of Fas ligand upregulation reveals a novel immunoregulatory consequence of CD4 ligation that might play a role in HIV infection and in the therapeutic application of anti-CD4 mAb.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
159
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
5742-9
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1997
pubmed:articleTitle
Ligation of cell surface CD4 inhibits activation-induced death of human T lymphocytes at the level of Fas ligand expression.
pubmed:affiliation
Department of Immunology, Paul Ehrlich Institute, Langen, Germany.
pubmed:publicationType
Journal Article