PubMed · 7532920
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K W Berean, J X O'Connell, V Tron. 1995. CD-34 expression.. https://doi.org/10.1097/00000478-199503000-00017
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Resting peripheral blood mononuclear cells (PBMC) or purified T-cells can be induced to proliferate when cocultured in vitro with fixed HTLV-infected T-cells. This process of HTLV-dependent cellular activation and induction of proliferation has been considered distinctive because of an apparent independence from conventional T-cell costimulatory signals. We have examined several HTLV-infected cell lines and found that proliferation was readily induced in resting PBMC by T-cells that were productively-infected with HTLV. However, equivalent HTLV-productive infection in a B-cell line failed to induce proliferation in PBMC, suggesting that HTLV-dependent induction of proliferation in PBMC was, at least in part, dependent upon a T-cell-specific signal. Furthermore, the induction of proliferation in PBMC populations was found to overlap with, and actually require, transfer and establishment of HTLV infection within the T-cell compartment of the PBMC population. These findings suggest that virus-induced activation of target cells may be directly associated with transfer and spread of HTLV infection.
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Following challenge of the acute promyelocytic leukemia (APL) cell line, NB4, with 1, 25 dihydroxy vitamin D3 (1, 25 D3), no increase in the expression of the monocytic surface markers, CD11c, CD14 and HLA-DR is observed. By contrast, 1, 25 D3 increases the expression of CD11b, an early myeloid marker and enhances adherence to plastic following priming of the cells with phorbol 12-myristate 13-acetate (PMA). NB4.306 and NB4.007/6, two all-trans retinoic acid-resistant cell lines originated from NB4 promyelocytes and lacking expression of a complete form of PML-RAR, are totally resistant to 1, 25 D3-dependent induction of CD11b. In addition, NB4.306 cells do not show enhanced plastic adherence following treatment with the vitamin D metabolite and PMA. NB4 and NB4.306 express similar amounts of the transcripts coding for the vitamin D3 receptor and the retinoid accessory receptors, RXR alpha and RXR beta, both in basal conditions and upon treatment with 1, 25 D3.