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PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1987-8-28
pubmed:abstractText
Human T cells exposed to high concentrations of influenza A virus cause specific suppression of the in vitro antibody response to the virus, but the phenomenon does not require viable T cells. In order to investigate the mechanism of this form of suppression, IL-2-dependent T cell clones of helper phenotype (CD4+, HLA-DR+, IL-2R+) were prepared with specificity for influenza A (Mem/Bel) and B (B HK) viruses and the non-crossreacting antigen purified protein derivative (PPD). When pulsed with high dose Mem/Bel virus, all three clones transferred suppression equally well to effector cultures of syngeneic or allogeneic E+ and E- cells stimulated with an immunogenic dose of the same virus. Thus, although suppression was specific at the level of expression, the induction phase was non-specific and non-major histocompatibility complex (MHC) restricted and did not involve interaction of antigen with the T cell receptor. HLA-DR, CD3 and CD8 determinants were excluded as the binding site for the virus by two-colour immunofluorescent staining and flow cytometric analysis. The concentrations of antigen required for high dose suppression inhibited antigen-specific proliferation by the clones; on the other hand, they remained partially sensitive to IL-2 and could still release gamma-interferon. These findings suggest that this phenomenon is distinct from conventional antigen-specific suppression mediated by CD8 T cells, but may play a biologically important role in regulating immune responses at least to viral antigens.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0818-9641
pubmed:author
pubmed:issnType
Print
pubmed:volume
65 ( Pt 1)
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
25-33
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1987
pubmed:articleTitle
High dose suppression of human anti-influenza A virus responses using T cell clones.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't