Biomedical subjects
M Macy
Publications and source records attributed to M Macy.
WiDr is a derivative of another colon adenocarcinoma cell line, HT-29.
This paper documents chromosomal and isozymic evidence indicating that WiDr is a derivative of another colon adenocarcinoma cell line, HT-29, which was established in 1964. The phenotypes for seven isozymes studied were identical for all HT-29 and WiDr cell lines. The karyotypes were similar between four HT-29 cultures separated by more than 100 passages and two WiDr cultures that were studied independently in 1979 and 1985. The isozymic and karyotypic data are consistent with that described for the cell line WiDr, originally reported in 1979. Detailed karyotypic comparisons further show that cultures of WiDr possess all nine chromosomal markers found in the initial HT-29 (passage 19) cultures. However, both the higher passaged HT-29 and WiDr differ from the initial HT-29 (passage 19) because it has an additional five to eight constitutive marker chromosomes. An increase or decrease of one copy in several normal chromosomes is also noticed with more normal chromosome gains than losses. The study provides another example demonstrating the remarkable karyotypic stability within a heteroploid cell line with continued passage. It also reemphasizes the critical need for detailed karyotypic and isoenzymic studies on all cell lines in common use.
Plasma lipoproteins and transferrin regulate the proliferation of a continuous T lymphocyte cell line.
Lipoproteins of hydrated densities less than 1.063 g/ml, very low density (VLDL) and low density (LDL) lipoproteins, could both enhance and suppress the proliferation of T lymphocyte cell lines. Enhancement and suppression were dependent on lipoprotein and transferrin concentrations. Enhancement occurred at low lipoprotein and high transferrin; suppression, at high lipoprotein and low transferrin. Lipoprotein suppression required a constituent of cell-conditioned medium as evidenced by the fact that lipoproteins did not suppress the replicative response of the IL-2-dependent murine cell line CTLL-2 to purified IL-2 but could suppress the response to cell-conditioned medium IL-2. For lipoprotein suppression and its relief by transferrin, both growth-regulating factors were required early in the cell cycle, suggesting that events important to progression through G1 are influenced. The data establish that the interplay between plasma lipoproteins, transferrin, and an unknown constituent of cell-conditioned medium can regulate the proliferation of T lymphocytes.
Plasma lipoproteins can suppress accessory cell function and consequently suppress lymphocyte activation.
The low density classes of plasma lipoproteins (d less than or equal to 1.063 g/ml) suppress mitogenic activation and proliferation of peripheral blood T lymphocytes. Here we demonstrate that lipoprotein suppression can be directed against the accessory cells (greater than 85% monocytes) required for optimal activation of lymphocytes by polyclonal mitogens. Preincubation of accessory cells for 24 h with very low (VLDL) and low (LDL) density lipoproteins suppressed their ability to enhance lymphocyte activation, whereas preincubation of T lymphocytes with lipoproteins did not alter their responsiveness to mitogens. The phenotypic distribution of the accessory cell population was not specifically altered by the lipoproteins, nor did loss of viability account for the suppressive effect of the lipoproteins. Furthermore, the lipoprotein-preincubated accessory cells did not secrete stable inhibitory substances, nor was their ability to produce interleukin 1 diminished. The results of mixing experiments indicate that VLDL-incubated accessory cells had not differentiated into suppressor cells. The lipoprotein-incubated accessory cells appeared to induce the interleukin 2-responsive state in the mitogen-activated lymphocytes, but could not deliver a signal or signals required for the further progression of the activated lymphocytes through the cell cycle. These important findings define at least two types of accessory cell function in the in vitro activation of T lymphocytes.
Accessory cells reduce lipoprotein suppression of lymphocyte activation.
Plasma lipoproteins of d less than or equal to 1.063 g/ml suppress lymphocyte activation triggered in vitro by polyclonal T cell mitogens. The extent of suppression decreases as the number of accessory cells per culture increases. Accessory cells isolated by glass adherence and by counter-flow centrifugation reduce lipoprotein suppression to the same extent. Modulation of lipoprotein suppression by accessory cells is independent of the amount and type of polyclonal activator. Reduction of lipoprotein suppression requires viable accessory cells and that they be present with lymphocytes, mitogen and lipoproteins during the initial 24-h culture period. It is within this same time period that lipoproteins exert their suppressive effect. Accessory cells isolated from a patient with the homozygous form (receptor-defective) of familial hypercholesterolemia also reduce the extent of lipoprotein suppression, suggesting that modulation is not mediated by the classic low density lipoprotein receptor. There appear to be at least two mechanisms by which accessory cells may alter lipoprotein suppression of T lymphocyte activation: by secretion of a soluble factor, probably not interleukin 1, that decreases the extent of suppression and by direct modification of the population of suppressive lipoproteins. Neither mechanism accounts for the lipoprotein-enhanced activation that occurs when cultures contain approximately equal numbers of T lymphocytes and accessory cells.
Certified cell lines of rat origin appear free of infection with Hantavirus.
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Suppression of lymphocyte activation by plasma lipoproteins: modulation by cell number and type.
Plasma lipoproteins containing apolipoproteins B and E, as well as delipidated water-soluble apoE, suppress lymphocyte activation by polyclonal T cell mitogens in vitro. This report establishes that apoB100, isolated from human plasma LDL, also suppresses lymphocyte activation. Prereplicative mitogen-induced events as well as DNA synthesis and cell division are suppressed. A number of experimental variables influence the extent to which lipoproteins suppress lymphocyte activation. Lipoproteins isolated from different donors vary widely in suppressive potency. In addition, the extent of suppression depends on the cultured cell density: suppression at fixed concentration of lipoprotein or apolipoprotein decreases as the number of cells increases. When the total number of cells per culture and the suppressor concentration are both fixed, the extent of suppression decreases as the percent T cells or monocytes increases. In the lymphatic tissue where lymphocytes and accessory cells are concentrated, plasma lipoproteins may play a less important immunoregulatory role in normolipidemic subjects compared to that in subjects with hyperlipoproteinemia, particularly hypercholesterolemia, since the tissue concentration of lipoproteins in hyperlipidemic subjects is likely to be elevated.
Bacteria with defective rho factors suppress the effects of N mutations in bacteriophage lambda.
A prediction based on the model for N-gene function of bacteriophage lambda proposed by Roberts (1971) is confirmed by showing that a lambdaN- double mutant is able to grow in strains of E. coli with defective rho transcription termination factors. The burst sizes for lambdaN- in these strains range from 5 to 24% the burst sizes for lambdaN+ in the same strain. This low level of suppression is also evident in the levels of synthesis of the lambda exonuclease and is consistent with other evidence that the defect in the rho factors of these strains is only partial. These strains do not suppress the effects of mutations in genes O, P and Q of lambda nor in genes 30 and 43 of bacteriophage T4. The lack of suppression of lambdaQ- is significant because the Q-gene product, like the N-gene product, is believed to function as an anti-terminator of lambda transcription but at termination sites that may not require rho factor action.