Linked Life Data

6306107

Source:http://linkedlifedata.com/resource/pubmed/id/6306107

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1983-8-26
pubmed:abstractText
Diminished regulation of EBV-induced B cell proliferation by T cells from patients with rheumatoid arthritis (RA) is paralleled by diminished production of gamma-interferon in response to autologous but not allogeneic stimulation. We have shown that the adherent cell subpopulation within the autologous RA stimulators plays a major role in the RA defect. In analyzing the mechanisms responsible for the adherent cell effect in RA, we examined the contribution of prostaglandin production. Indomethacin treatment (1 microgram/ml) of the RA auto-MLR led to increased production of supernatant inhibitory activity (8% +/- 4 without, 57% +/- 4 with indomethacin), but had no significant effect on the inhibition of EBV-induced B cell proliferation by normal auto-MLR supernatants. Adding excess autologous adherent cells to the normal auto-MLR, however, led to an indomethacin-reversible decline in the production of the inhibitory factor without suppressing the auto-MLR proliferative response. The adherent cell effect could be reproduced by adding PGE1 or PGE2 (10(-8) to 10(-6) M) to the normal auto-MLR. PGE2 levels in 72-hr auto-MLR supernatants were similar in RA (4.2 +/- 1 ng) and normal control (3.6 +/- 0.5 ng/ml) supernatants. Because we could not detect differences in PGE production, we assessed the sensitivity of adherent cell-depleted normal and RA auto-MLR to exogenous PGE. Concentrations of 10(-7) to 10(-6) M PGE were needed to block production of the inhibitory factor by to normal cells, whereas only 10(-13) to 10(-12) M PGE1 completely blocked it in RA cell cultures. Thus, the defective production of gamma-interferon in the RA auto-MLR is, at least in part, due to enhanced sensitivity of the RA lymphocytes to adherent cell-produced prostaglandins.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:volume
131
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
768-72
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
Analysis of the defects responsible for the impaired regulation of EBV-induced B cell proliferation by rheumatoid arthritis lymphocytes. II. Role of monocytes and the increased sensitivity of rheumatoid arthritis lymphocytes to prostaglandin E.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't