作者: CS Chan , F Soehnlen , GP Schechter
DOI: 10.1182/BLOOD.V76.8.1601.1601
关键词:
摘要: We examined in vitro tritiated thymidine uptake by B cells from seven prolymphocytic leukemia (PLL), chronic lymphocytic (CLL), and four plasma cell (PCL) patients response to culture with anti-human IgM antibody (anti-mu) B-cell growth factor (BCGF). In contrast the stimulatory effect observed normal cultures, divalent F(ab')2 anti-mu uniquely inhibited autonomous proliferation induced marked cytotoxicity six of PLL cultures independent complement or Fc-receptor-mediated mechanisms. There was neither stimulation inhibition slgM+ CLL slgM- PCL cells. The inhibitory on at an concentration below threshold for Significant impairment trypan blue exclusion delayed until 48 hours, morphological cellular changes suggestive a programmed death mechanism apoptosis. slgM-staining intensity BCGF-augmented DNA synthetic activity similar de novo transformation CLL. Cells patient were separated elutriation into two fractions, BCGF-unresponsive large "transformed" fraction synthesis smaller lymphoid subset low 3H-thymidine that could be augmented BCGF. Both fractions equally susceptible cytotoxic anti-mu. These data suggest certain slgM-bearing malignant are anti-mu-triggered cytotoxicity. They may represent counterpart "tolerogenic" subset, unique direct provide therapeutic strategy specifically PLL.