Linked Life Data

3500976

Source:http://linkedlifedata.com/resource/pubmed/id/3500976

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pubmed-article:3500976pubmed:abstractTextWe have recently described three "immature" B cell lymphomas which are exquisitely sensitive to growth inhibition by anti-Ig reagents and may serve as models for tolerance induction in normal B cells. These cells are inhibited from cell cycle progression into S after receiving a negative signal in early G1. In this paper, we demonstrate that the growth inhibition by anti-Ig can be prevented and reversed by the addition of supernatants from T cell lines. One such line, called Tova, produces factors which restore normal levels of DNA synthesis in the presence of concentrations of anti-Fab or anti-kappa immunoglobulins which cause up to a 90% inhibition of thymidine incorporation in a 2- to 3-day culture period. This factor is at least partially effective when added up to 24 hr after anti-Ig to unsynchronized lymphoma cells and it does not alter the growth of control cultures. Studies using synchronized lymphoma cells indicated that the T cell factor permitted cycle progression into S when added during the early G1 exposure to anti-kappa and was less effective when added late in G1. Preliminary characterization suggests that both B cell growth factor II (interleukin 5) and B cell stimulatory factor 1 (interleukin 4) have additive activity in this system, although another unidentified lymphokine may also be involved. The relevance of T cell reversal of Ig receptor-mediated negative signaling to neonatal B cell tolerance is emphasized.lld:pubmed
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pubmed-article:3500976pubmed:authorpubmed-author:KlausG GGGlld:pubmed
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pubmed-article:3500976pubmed:pagination3924-9lld:pubmed
pubmed-article:3500976pubmed:dateRevised2006-11-15lld:pubmed
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pubmed-article:3500976pubmed:year1987lld:pubmed
pubmed-article:3500976pubmed:articleTitleLymphoma models for B cell activation and tolerance. VI. Reversal of anti-Ig-mediated negative signaling by T cell-derived lymphokines.lld:pubmed
pubmed-article:3500976pubmed:affiliationDivision of Immunology, National Institute for Medical Research, London, England.lld:pubmed
pubmed-article:3500976pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3500976pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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