Extracts of hamster-human and mouse-human hybrids, some with translocations involving chromosome 19, have been assayed for both human spleen ferritin (rich in L subunits) and human heart ferritin (rich in H subunits). Hybrid lines retaining part of the long arm of chromosome 19 including the region 19q13.3----19qter produced human "L" type ferritin. This confirms the previous assignment of the "ferritin gene" to chromosome 19 (Caskey et al. 1983). However, lines retaining chromosome 11 were found to contain human "H" type ferritin suggesting that the gene for the "H" subunit is on this chromosome. The presence of chromosome 6 was not necessary for the expression of either "H" or "L" type human ferritin. It thus seems unlikely that the gene for idiopathic haemochromatosis is a ferritin gene.
SUMMARYTwo different subsets of CD8+, CD57+ cells have been defined, one expressing high levels (CD8W0+(CD57+)), the other expressing low levels of surface CD8 (CD81o0+(CD57+)). Increased numbers of CD8,gh+(CD57+) cells correlated with previous HCMV infection. By three-colour fluorescence analysis, the CD8high+(CD57+) population expressed T cell markers such as CD3 and CD5, and most were axf T cell receptor (afi TCR)-positive. A significant proportion also expressed CD71 (transferrin receptor) and MHC class II, although little if any CD25 (IL-2R-p55). Some ( > 40%) co-expressed CD45RA and CD45RO. The CD810,+(CD57+) population expressed classical natural killer (NK) cell markers-CD2, CD16 and CD56. The two subsets were also functionally distinct; CD8,gh+(CD57+) cells suppressed pokeweed mitogen (PWM)-driven, but not phytohaemagglutinin (PHA)-driven proliferation and immunoglobulin production; CD81,w+(CD57+) cells exhibited NK cytotoxic activity which was not increased by interferon-alpha (IFN-a). Supernatant from cultured CD8igh+(CD57+) cells suppressed PWM-driven immunoglobulin production, but not proliferation, and this effect was abrogated by physical separation with tissue culture inserts. Thus, a T cell subset expressing activation and memory T cell markers with direct non-specific suppressor activity was present in peripheral blood mononuclear cells (PBMC) of healthy subjects with asymptomatic HCMV infection.
We have used 25 sets of oligonucleotide primers specific for the 24 known major human T-cell receptor (TCR) V beta families in polymerase chain reactions to analyse the T-cell repertoire of the peripheral blood in seven patients with chronic myeloid leukaemia (CML). In contrast to normal healthy individuals, all seven patients exhibited variable degrees of TCR V beta-specific T-cell deletion, ranging from two to eight of the 24 major families. T cells bearing V beta 17 and 8 were most commonly deleted. These results suggest a superantigen effect associated with CML. The patterns of deletion did not appear to correlate with either of the two bcr-abl transcripts. The reason and aetiological agent responsible for the T-cell deletion remain speculative. Further work is ongoing to characterize this phenomenon in animal models and patients with CML.
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