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T Leanderson

Publications and source records attributed to T Leanderson.

81 records · Page 5Linked to original sources
PubMed1985

Mycoplasma mimicry of lymphokine activity in T-cell lines.

During screening of T-T hybridomas for B-cell-stimulating factors (BSF) we found in the conditioned medium of such a line (TUH-14) an activity that turned out to cosediment with a contaminating strain of Mycoplasma arginini on centrifugation. Since it only affected B blasts and only to a minor extent small cells and since it did not induce immunoglobulin secretion, the mycoplasma strain seemed to mimic a BSF. M. arginini was also found in two other T-T hybridoma producer lines but not in a clone of the EL-4 line. Three other M. arginini isolates were not stimulatory for B cells. The presented results point towards the importance of careful control for mycoplasma contamination in established cell lines.

Animals↗
PubMed1984

Effects of mu-specific antibodies on B cell growth and maturation.

Over a wide range of concentrations affinity-purified rabbit anti-mouse mu chain antibodies, or their F(ab')2 fragments, inhibit the appearance of immunoglobulin-secreting cells (plaque-forming cells; PFC) in lipopolysaccharide-stimulated murine spleen cell cultures without affecting proliferation. Both IgM and IgG PFC are inhibited although the number of blasts bearing surface IgG remains unaltered. The IgM and IgG PFC response could be reconstituted to normal levels in cell cultures suppressed by mu-specific antibodies by the addition of supernatants from in vitro propagated helper T cell clones, or from EL4 lymphoma cells induced with phorbol ester. Interleukin 1-containing P388 supernatant, or recombinant DNA-derived murine interferon-gamma, did not reconstitute the PFC response in cell cultures suppressed by mu-specific antibodies, indicating that other factors are responsible for these effects. When spleen cell cultures, pre-activated with either lipopolysaccharide or monoclonal mouse mu-specific antibodies coupled to Sepharose, were exposed to EL4 supernatants in the presence of soluble mu-specific antibodies, maturation to secretion was inhibited while proliferation was not. The implications of these findings on assay systems for B cell growth and maturation factors are discussed.

Animals↗
PubMed1984

Interferon-induced cell cycle changes in human hematopoietic cell lines and fresh leukemic cells.

A panel of 26 human hematopoietic cell lines was tested for sensitivity to growth inhibition towards interferon-alpha (IFN-alpha) by estimating the effects on cell cycle phase distribution using flow cytometry analysis. The proportion of proliferating cells was assessed by studying the fractional increase of cells in mitosis during a 24-hr vinblastine block. Of 26 cell lines tested, 17 were sensitive to IFN-alpha, and the main cell cycle effect was accumulation in the G0-G1 phase. One Burkitt's lymphoma line, Namalwa, showed a decreased rate of progress through S without any G0/G1 accumulation. Three of the cell lines were also tested with IFN-beta and with IFN-alpha 2 produced by recombinant DNA technology. The latter IFN did not affect one of the cell lines; otherwise, the results were similar to those of IFN-alpha. Six of 16 clinical specimens from patients with hematopoietic neoplasias were IFN-sensitive, all displaying a G0-G1 block. Our results indicate that IFN sensitivity is an individually linked property unrelated to cell origin.

Cell Cycle↗
PubMed1982

Interferon-specific effects on protein synthesis in P3HR-1 cells.

The effect of interferon (IFN) on protein synthesis was studied in the Burkitt's lymphoma cell line P3HR-1 by [35S]methionine labelling of the cells, followed by two-dimensional gel electrophoresis of cell extracts. De novo synthesis of three proteins (mol. wts. 33 000, 62 000, and 98 000, respectively) and alterations in the rate of synthesis for a small number of additional proteins were observed during the first 12 h of treatment, while the rate of overall protein synthesis was unaffected. Treatment of P3HR-1 cells with 12-O-tetradecanoyl-phorbol-13-acetate (TPA) or hydrocortisone (HC), which induce similar changes in cell cycle distribution as does IFN, did not induce comparable changes in the rates of protein synthesis. Thus, the effects were specific for IFN and not induced by the change in cell cycle distribution per se, i.e., accumulation in G0. Treatment of cells with 2'-5' pA core did not mimic the effect of IFN at the translational level. A substrain of P3HR-1 cells, selected for resistance to the anti-proliferative effect of IFN, lacked six proteins found in the wild-type. The 62 000 mol. wt. protein was induced in this substrain as well as in native P3HR-1 cells on addition of IFN. The resistant substrain still developed an anti-viral effect in response to IFN. Thus, it seems as if the anti-proliferative and anti-viral effects of IFN, at least in some cells are mediated by different intracellular molecular mechanisms.

Burkitt Lymphoma↗
PubMed1982

B-cell growth factor: distinction from T-cell growth factor and B-cell maturation factor.

A T-cell hybridoma was derived by somatic cell hybridization between concanavalin A-activated BALB/c spleen cells and the AKR thymoma BW 5147. Media conditioned by hybridoma cells, even at high dilutions (1:1,000) support the growth of lipopolysaccharide-stimulated B-cell blasts but not that of T-cell growth factor (TCGF)-reactive T-cells. This activity, herein designated B-cell growth factor (BCGF), has a Mr of approximately equal to 20,000 and it can readily be separated from TCGF (Mr approximately equal to 30,000) by gel filtration. BCGF is constitutively produced by the hybridoma cells, it is removed from conditioned media by incubation with target cells at +4 degrees C, and it is equally effective on B-cell blasts carrying different major histocompatibility complex and Ig haplotypes. BCGF shows no T-cell replacing factor (TRF) activity, and it is poor in supporting the development of Ig-secreting plaque-forming cells in B-cell blast cultures. Terminal maturation, however, can be induced in BCGF-dependent blasts by addition of conditioned media from normal helper T cell cultures, suggesting that two distinct factors are involved in the helper cell-dependent growth and maturation of B lymphocytes.

Animals↗
PubMed1982

Growth inhibition by IFN achieved by collecting cells in G0.

The P3 HR-1 cell line was studied with respect to sensitivity to the growth inhibitory properties of Hu IFN-alpha (leukocyte interferon). Cells growth arrested at high density and diluted into fresh medium, were growth inhibited at the same time and to the same degree as exponentially growing cells. Thus, resting cells did not seem to be more sensitive to IFN than exponentially growing cells. The cells displayed the same sensitivity to IFN during all cell cycle phases and they were found to enter the G0 stage in a dose dependent manner following first order kinetics.

Burkitt Lymphoma↗
PubMed1982

Selective effects of interferon on distinct sites of the T lymphocyte triggering process.

Lectin- and antigen-induced proliferation of murine T cells consists of two major events, namely, a rapid induction of susceptibility to growth factors and a later-occurring, accessory cell-dependent production of T cell growth factors (TCGF). The mechanism by which interferon (IFN) inhibits T cell responses was studied accordingly. A decrease of Con A-induced proliferation was observed in the presence of increasing amounts of IFN. The reduced proliferative response in such cultures was found to be due to an accumulation of cells in the G0/G1 phase of the cell cycle. Furthermore, the results show that IFN did not inhibit the early events in T cell triggering, because the acquisition of responsiveness of resting T cells to TCGF was unaltered in the presence of IFN, nor did it interfere with production of TCGF. In contrast, IFN was found to interfere with the TCGF-dependent T cell blast growth. Cytofluorometric analysis of the proliferative phase revealed that IFN exerts its effect on T cells, which have entered the proliferative cycle, by a postmitotic accumulation in G0/G1, thus reducing the proliferating population. The results demonstrate that IFN primarily affects the later phase of proliferative activity after T cell triggering, leaving the helper cell functions untouched.

Animals↗
PubMedDate not supplied

Mitogenic effects of phorbol myristate acetate (PMA) on amphibian cells.

Tumour promoter phorbol myristate acetate (PMA) stimulates and causes proliferation of cells from the spleen, thymus and peripheral blood of Xenopus laevis, the clawed toad. Phagocytic cells become activated and from foci of clustered cells. B cells blast and change membrane immunoglobulin (Ig) expression; a small portion go on to secrete Ig. The surface Ig-negative splenocyte population, which contains T cells, responds to PMA by active proliferation. Splenocytes, once stimulated by PMA, become refractory to further addition of PMA but respond instead to ConA. These results are discussed in the general context of the effect of PMA lymphocytes.

Animals↗