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Journal articles on the topic 'Proliferate'

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Published: 10 December 2022

Last updated: 28 January 2023

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1

Matsue, H., P. R. Bergstresser, and A. Takashima. "Keratinocyte-derived IL-7 serves as a growth factor for dendritic epidermal T cells in mice." Journal of Immunology 151, no. 11 (December 1, 1993): 6012–19. http://dx.doi.org/10.4049/jimmunol.151.11.6012.

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Abstract Dendritic epidermal T cells (DETC) are CD3+, CD45+, CD4-, CD8-, TCR-V gamma 3/V delta 1+ T lymphocytes that reside in symbiosis with keratinocytes in mouse epidermis. To address mechanisms by which these cells survive and proliferate within the epidermal environment, we have tested the hypothesis that cytokines secreted by neighboring keratinocytes play relevant roles. The present study was conducted to determine whether keratinocytes produce biologically relevant amounts of IL-7, and, if so, to study its effects on DETC. The long term cultured DETC line, 7-17, and freshly isolated DETC exhibited dose- and time-dependent proliferative responses to rIL-7. These responses were blocked completely by anti-IL-7 antibodies, whereas anti-IL-2 had no effect, indicating that DETC respond to IL-7 by an IL-2-independent mechanism. Proliferative responses depended on the state of cell activation; DETC stimulated 2 to 5 days earlier with Con A proliferated optimally to added IL-7, whereas cells stimulated 10 days earlier did not proliferate. DETC that failed to proliferate responded to IL-7 by showing prolonged survival; cells maintained for 7 days with IL-7 alone retained their capacity to proliferate in response to Con A. Mouse epidermal cells and Pam 212 keratinocyte line both expressed IL-7 mRNA constitutively, as demonstrated by reverse transcription-polymerase chain reaction analyses. The production of IL-7 by mouse keratinocytes was also confirmed; Pam 212 culture supernatants supported DETC proliferation, and this activity was diminished by 50% with added anti-IL-7 antibodies. These results indicate that keratinocytes produce IL-7 in biologically relevant amounts, which, in turn, serve to promote the survival and growth of DETC. IL-7-mediated communication between epithelial cells and gamma delta T cells may represent one mechanism to sustain the indefinite residence of gamma delta T cells in epithelial tissues of mice.

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2

Dempsey, E. C., I. F. McMurtry, and R. F. O'Brien. "Protein kinase C activation allows pulmonary artery smooth muscle cells to proliferate to hypoxia." American Journal of Physiology-Lung Cellular and Molecular Physiology 260, no. 2 (February 1, 1991): L136—L145. http://dx.doi.org/10.1152/ajplung.1991.260.2.l136.

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Pulmonary artery (PA) smooth muscle cell (SMC) proliferation occurs with hypoxic pulmonary hypertension in vivo. However, proliferation of cultured PA SMC to hypoxia has not been demonstrated, and thus the mechanism by which these cells respond to hypoxia is unknown. Because protein kinase C (PKC) plays a role in intracellular transduction of proliferative signals, we asked whether PKC activation 1) causes proliferation of bovine PA SMC and 2) is important in PA SMC proliferative response to hypoxia. By measuring [3H]thymidine incorporation and cell counts, we found that quiescent PA SMC from four different cows proliferated with the PKC activator, phorbol 12-myristate 13-acetate (PMA), in a concentration-dependent manner. The proliferation was blocked with a PKC inhibitor, dihydrosphingosine, or by downregulating SMC PKC. We tested whether “priming“ PA SMC by PKC activation was required for in vitro SMC proliferative response to hypoxia. Each SMC population was treated with PMA and then exposed for 24 h to 20, 10, 7, 3 or 0% O2. These cells proliferated with hypoxia reaching a peak response at 3% O2. The magnitude of the response to PMA and hypoxia was different for each cell population tested. No hypoxic proliferation occurred in control cells (no PMA). Dihydrosphingosine blocked the hypoxic response to the same extent that it inhibited the initial PMA conditioning stimulus. PKC-downregulated PA SMC did not proliferate to PMA or to subsequent hypoxia. The hypoxic response was not due to a reduction in O2 radical-mediated antiproliferative effect; rather, the PMA-primed cells seemed to “acquire” the ability to directly sense hypoxia and proliferate. In summary, PKC activation caused proliferation of PA SMC in vitro and allowed an additional proliferative response to hypoxia. Activation of PKC may be a requisite step for PA SMC to respond directly to hypoxia.

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3

Turco, MC, M. De Felice, F. Alfinito, A. Lamberti, F. Costanzo, M. Giordano, V. Martinelli, B. Rotoli, S. Ferrone, and S. Venuta. "Proliferative pathways in CD1- CD3+ CD4+ CD8+ T-prolymphocytic leukemic cells: analysis with monoclonal antibodies and cytokines." Blood 74, no. 5 (October 1, 1989): 1651–57. http://dx.doi.org/10.1182/blood.v74.5.1651.1651.

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Abstract The antigenic profile and the proliferative pathways in leukemic cells from the patient TRT with T-prolymphocytic leukemia (T-PLL) were analyzed using monoclonal antibodies (MoAbs) and cytokines. T-PLL cells expressed the phenotype CD1- CD3+ CD4+ CD8+. Incubation with the differentiating agent phorbol-12-myristate-13-acetate markedly increased the percentage of cells with the CD4- CD8+ phenotype, suggesting that leukemic cells were already committed towards a differentiated element with the CD4- CD8+ phenotype. T-PLL cells were induced to proliferate by anti-CD2 MoAb 9–1 + 9.6 and by anti-CD3 MoAb OKT3. The two pathways exhibited normal functional interactions and were susceptible to modulation by anti-HLA class I MoAbs. These results indicate that regulation of cell proliferation was preserved to a significant extent in the T-PLL cells analyzed. At variance with normal resting T cells that require previous activation to proliferate when incubated with interleukin-1 (IL-1) or interleukin-2 (IL-2), T-PLL cells proliferated vigorously when incubated with either interleukin. Furthermore, T-PLL cells proliferated when incubated with immune interferon (IFN-gamma). The latter finding parallels the enhancement by IFN-gamma of the proliferative response of lectin-activated murine T lymphocytes. These results suggest that T-PLL cells, which express a high constitutive level of c-myc mRNA, may be in an activated state. The antigenic phenotype and the characteristics of the proliferative pathways of T-PLL cells from the patient TRT are compatible with the possibility that they may be derived from an intermediate thymocyte.

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4

Turco, MC, M. De Felice, F. Alfinito, A. Lamberti, F. Costanzo, M. Giordano, V. Martinelli, B. Rotoli, S. Ferrone, and S. Venuta. "Proliferative pathways in CD1- CD3+ CD4+ CD8+ T-prolymphocytic leukemic cells: analysis with monoclonal antibodies and cytokines." Blood 74, no. 5 (October 1, 1989): 1651–57. http://dx.doi.org/10.1182/blood.v74.5.1651.bloodjournal7451651.

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The antigenic profile and the proliferative pathways in leukemic cells from the patient TRT with T-prolymphocytic leukemia (T-PLL) were analyzed using monoclonal antibodies (MoAbs) and cytokines. T-PLL cells expressed the phenotype CD1- CD3+ CD4+ CD8+. Incubation with the differentiating agent phorbol-12-myristate-13-acetate markedly increased the percentage of cells with the CD4- CD8+ phenotype, suggesting that leukemic cells were already committed towards a differentiated element with the CD4- CD8+ phenotype. T-PLL cells were induced to proliferate by anti-CD2 MoAb 9–1 + 9.6 and by anti-CD3 MoAb OKT3. The two pathways exhibited normal functional interactions and were susceptible to modulation by anti-HLA class I MoAbs. These results indicate that regulation of cell proliferation was preserved to a significant extent in the T-PLL cells analyzed. At variance with normal resting T cells that require previous activation to proliferate when incubated with interleukin-1 (IL-1) or interleukin-2 (IL-2), T-PLL cells proliferated vigorously when incubated with either interleukin. Furthermore, T-PLL cells proliferated when incubated with immune interferon (IFN-gamma). The latter finding parallels the enhancement by IFN-gamma of the proliferative response of lectin-activated murine T lymphocytes. These results suggest that T-PLL cells, which express a high constitutive level of c-myc mRNA, may be in an activated state. The antigenic phenotype and the characteristics of the proliferative pathways of T-PLL cells from the patient TRT are compatible with the possibility that they may be derived from an intermediate thymocyte.

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5

Lee, Y. "To proliferate or not to proliferate." Cardiovascular Research 86, no. 3 (April 7, 2010): 347–48. http://dx.doi.org/10.1093/cvr/cvq107.

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6

Gilbert, K. M., K. D. Hoang, and W. O. Weigle. "Th1 and Th2 clones differ in their response to a tolerogenic signal." Journal of Immunology 144, no. 6 (March 15, 1990): 2063–71. http://dx.doi.org/10.4049/jimmunol.144.6.2063.

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Abstract Th1 and Th2 clones specific for human gamma globulin (HGG) were compared and shown to differ in terms of the effects of tolerance induction on Ag-induced proliferation and helper activity. In developing a method to induce tolerance, splenic APC that had been pulsed with HGG and then fixed with 0.15% paraformaldehyde (HGG-FAPC) were used as a means to present Ag to the Th clones in the absence of costimulatory signals. Both Th1 and Th2 clones recognized HGG-FAPC as evidenced by their ability to proliferate to HGG-FAPC. Unlike Th2, Th1 proliferated to HGG-FAPC only in the presence of T cell-depleted allogeneic spleen cells as a source of accessory cell signals. The inability of Th1 cells to proliferate in the absence of costimulatory signals was due to Ag-specific inactivation: Th1 clones preincubated with HGG-FAPC were unable to proliferate when recultured with HGG and irradiated APC. In contrast to Th1 clones, Th2 clones showed no decrease in their Ag-induced proliferative capacity after exposure to any concentration of HGG-FAPC. However, when examined by using a second assay system, that of providing help for anti-HGG antibody production by primed B cells, Th2 preincubated with HGG-FAPC were markedly inhibited (up to 90%) in their ability to provide help. Preincubation with HGG-FAPC also inhibited the helper activity of the one Th1 clone that was found to induce a significant secondary antibody response. Taken together, the results suggest that exposure of Th1 to tolerogen in the form of HGG-pulsed fixed APC inactivates Th1 proliferative capacity, and possibly Th1 helper activity as well. Exposure of Th2 cells to a tolerogen suppresses the mechanism by which the Th2 cells provide Ag-induced B cell help, but does not inhibit the mechanism by which they proliferate to HGG. Furthermore, the results define a model that incorporates Ag processing as well as Ag presentation in the induction of tolerance in vitro.

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7

Leiper, James M., M. Birdsey Graeme, and Paru B. Oatey. "Peroxisomes proliferate." Trends in Cell Biology 5, no. 11 (November 1995): 435–37. http://dx.doi.org/10.1016/s0962-8924(00)89103-5.

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8

Stajic, Jelena. "Triplets Proliferate." Science 336, no. 6077 (April 5, 2012): 13.1–13. http://dx.doi.org/10.1126/science.336.6077.13-a.

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9

Defrance, T., J. P. Aubry, B. Vanbervliet, and J. Banchereau. "Human interferon-gamma acts as a B cell growth factor in the anti-IgM antibody co-stimulatory assay but has no direct B cell differentiation activity." Journal of Immunology 137, no. 12 (December 15, 1986): 3861–67. http://dx.doi.org/10.4049/jimmunol.137.12.3861.

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Abstract In this study it is illustrated that recombinant human interferon-gamma (IFN-gamma) acts as a B cell growth factor (BCGF) in the anti-IgM antibody co-stimulatory assay. A monoclonal antibody that specifically inhibits the biological activities of IFN-gamma blocks its BCGF activity supporting the specificity of the IFN-gamma effect. Various IFN-gamma obtained from different sources displayed the same BCGF activity. Nonactivated B lymphocytes do not proliferate in response to IFN-gamma. IFN-gamma acts directly on B cells because highly purified B cells obtained after standard purification procedures coupled to cell sorting could still proliferate in response to IFN-gamma. Blood B lymphocytes were found to be more sensitive to the BCGF activity of IFN-gamma than B cells obtained from spleens or tonsils. The IFN-gamma-induced proliferation of B cells was short lasting when compared with that of recombinant IL 2 or BCGF containing T cell clone supernatants. B cells preactivated with either Staphylococcus aureus strain Cowan I (SAC) or optimal concentrations of anti-IgM antibodies coupled to beads did not proliferate in response to IFN-gamma, whereas they proliferated in response to IL 2 or T cell clone supernatants. IFN-gamma did not stimulate nor inhibit the proliferative response of human B lymphocytes stimulated with optimal concentrations of anti-IgM antibodies or SAC. Additionally none of the different IFN-gamma tested had B cell differentiation factor activity in the standard SAC assay. These results indicate that IFN-gamma sensitizes B cells to suboptimal mitogenic concentrations of anti-IgM antibody.

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10

Vallée, Isabelle, Jean-Maurice Guillaumin, Gilles Thibault, Yves Gruel, Yvon Lebranchu, Pierre Bardos, and Hervé Watier. "Human T Lymphocyte Proliferative Response to Resting Porcine Endothelial Cells Results from an HLA-Restricted, IL-10-Sensitive, Indirect Presentation Pathway But Also Depends on Endothelial-Specific Costimulatory Factors." Journal of Immunology 161, no. 4 (August 15, 1998): 1652–58. http://dx.doi.org/10.4049/jimmunol.161.4.1652.

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Abstract To investigate the mechanisms of cellular rejection in pig-to-human xenotransplantation, the proliferation of different human purified lymphocyte subpopulations in response to swine leukocyte Ag class II-negative porcine aortic endothelial cells (PAEC) was measured in the presence or absence of human autologous adherent cells (huAPC). CD8+ lymphocytes proliferated moderately in the absence of huAPC, and the immune response was slightly increased when huAPC were added. CD56+ lymphocytes failed to proliferate in response to PAEC whether huAPC were present or not. CD4+ lymphocytes alone did not proliferate in response to PAEC, but a strong proliferative response was observed in the presence of metabolically active huAPC. This response was totally abolished by mAbs directed against HLA class II molecules or by pretreatment of huAPC by human IL-10. Even in the presence of huAPC, CD4+ lymphocytes failed to respond to fixed PAEC or to PAEC-lysates, suggesting that PAEC must be viable to support lymphocyte proliferation. Finally, none of the nonendothelial porcine adherent cells tested was able to induce human lymphocyte proliferation, despite the fact that they also provided a large set of xenogeneic peptides. Our results show that the indirect presentation pathway of xenoantigens by huAPC to CD4+ lymphocytes is crucial in the response to porcine endothelial cells, and that IL-10 could be of therapeutic interest to prevent human lymphocyte activation by this pathway. Furthermore, we demonstrated that stimulatory signals specifically provided by endothelial cells are also necessary for this huAPC-restricted proliferative response.

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11

Sieckmann, D. G., K. Holmes, P. Hornbeck, E. Martin, G. Guelde, S. Bondada, D. L. Longo, and J. J. Kenny. "B cells from M167 mu kappa transgenic mice fail to proliferate after stimulation with soluble anti-Ig antibodies. A model for antigen-induced B cell anergy." Journal of Immunology 152, no. 10 (May 15, 1994): 4873–83. http://dx.doi.org/10.4049/jimmunol.152.10.4873.

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Abstract The transgenic (TG) mouse strain 207-4, carries mu a + kappa transgenes ligated to the anti-phosphocholine (PC) VH1 and V kappa 24 V region genes from the MOPC-167 myeloma. Although B cells from mice carrying these transgenes respond both in vivo and in vitro to thymus-dependent Ags, they failed to proliferate in response to soluble goat anti-mu Ab or other soluble anti-Ig reagents. On the other hand, B cells from the Sp6 mu kappa anti-trinitrophenyl TG mouse line proliferated normally after stimulation with soluble anti-mu. However, the 207-4 anti-PC transgene positive (TG+) splenic B cells proliferated when stimulated with anti-mu, anti-idiotype, anti-allotype, or PC-conjugated to Sepharose beads. TG+ B cells were also induced to proliferate when stimulated with anti-Lyb-2; thus, their defect may be restricted to signaling through sigM. The lack of response to soluble anti-mu could not be reversed by addition of IL-4, by removal of T cells, by addition of anti-FcR Ab, or by stimulation with F(ab')2 anti-mu. Thus, the failure to proliferate was not caused by active T cell suppression or FcR-mediated inhibition. In mixed cultures of TG+ and transgene negative (TG-) spleen cells, the TG- cells were able to proliferate normally to soluble anti-mu, indicating that suppressive factors were not involved in the unresponsiveness of the TG+ anti-PC-specific B cells. These studies suggest that B cells in the 207-4 anti-PC TG mice exhibit a defect in activation through their sIgM receptors, and this unresponsiveness may reflect a form of Ag-induced tolerance.

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12

Joglekar, Mugdha V., Vinay M. Joglekar, Sheela V. Joglekar, and Anandwardhan A. Hardikar. "Human fetal pancreatic insulin-producing cells proliferate in vitro." Journal of Endocrinology 201, no. 1 (January 26, 2009): 27–36. http://dx.doi.org/10.1677/joe-08-0497.

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There have been considerable efforts towards understanding the potential of human pancreatic endocrine cells to proliferate and transition into mesenchymal cell populations. Since rodent studies have demonstrated that mouse insulin-producing cells do not proliferate in vitro, a similar possibility has been considered for human islet endocrine cells. Considering the inherent differences in mouse and human pancreatic islets, we decided to assess the potential of human fetal pancreatic insulin-producing cells to proliferate in vitro. We studied the proliferative potential of human fetal pancreatic islet-derived populations from second or third trimester fetal pancreas and characterized the cells that grow out during their expansion. We have used seven different approaches including in situ hybridization and immunostaining, quantitative estimation of multiple gene transcripts in populations as well as in single cells, clonal analysis of islet cells, assessment of heritable marks of active insulin promoter, and thymidine analog-based lineage tracing. Our studies demonstrate that human fetal pancreatic insulin-producing cells proliferate in vitro to generate mesenchymal cell populations. Interestingly, epigenetic modifications that mark open chromatin conformation of insulin promoter regions are retained even after a million fold expansion/proliferation in vitro. These findings demonstrate that hormone-producing cells in pancreatic islets proliferate in vitro and retain epigenetic marks that characterize an active insulin promoter. Such in vitro-derived mesenchymal cells may be of potential use in cell-replacement therapy for diabetes.

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13

Van Brunt, Jennifer. "Interferon Trials Proliferate." Nature Biotechnology 7, no. 6 (June 1989): 549. http://dx.doi.org/10.1038/nbt0689-549b.

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14

Frede, J., and P. H. Jones. "Permission to Proliferate." Science 342, no. 6163 (December 5, 2013): 1183–84. http://dx.doi.org/10.1126/science.1248274.

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15

Schneider, David. "Plug-ins proliferate." IEEE Spectrum 49, no. 1 (January 2012): 36–37. http://dx.doi.org/10.1109/mspec.2012.6117832.

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16

Glaser, Vicki. "Screening Innovations Proliferate." Genetic Engineering & Biotechnology News 31, no. 10 (May 15, 2011): 1–21. http://dx.doi.org/10.1089/gen.31.10.07.

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17

WILKINSON, SOPHIE. "Proteomics Publications Proliferate." Chemical & Engineering News 79, no. 10 (March 5, 2001): 10. http://dx.doi.org/10.1021/cen-v079n010.p010a.

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18

Culotta, E. "Planetary Systems Proliferate." Science 286, no. 5437 (October 1, 1999): 65. http://dx.doi.org/10.1126/science.286.5437.65.

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19

Jespersen, Bjørn. "Should Propositions Proliferate?" Thought: A Journal of Philosophy 4, no. 4 (September 22, 2015): 243–51. http://dx.doi.org/10.1002/tht3.184.

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20

O'Nions, Jenny, and Martin J. Allday. "Proliferation and differentiation in isogenic populations of peripheral B cells activated by Epstein–Barr virus or T cell-derived mitogens." Journal of General Virology 85, no. 4 (April 1, 2004): 881–95. http://dx.doi.org/10.1099/vir.0.19704-0.

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Human B cells isolated from peripheral blood were activated and induced to proliferate by either Epstein–Barr virus (EBV) or the T cell-derived mitogens CD40 ligand (CD40L) plus interleukin (IL)-4. Although both populations initially proliferated as B-blasts, significant differences were revealed over a longer period. EBV infection resulted in continuously proliferating lymphoblastoid cell lines (LCLs), whereas most of the CD40L/IL-4-stimulated B cells had a finite proliferative lifespan of 3–4 weeks. Cell cycle analysis, trypan blue staining and Western blot analysis for cleavage of poly(ADP-ribose) polymerase (PARP) all demonstrated that the decrease in proliferation in CD40L/IL-4-stimulated B cells is not due to cell death. Instead, these cells arrest, accumulate in G0/G1 and undergo alterations in cell surface marker expression, cellular morphology and immunoglobulin production, all consistent with plasmacytoid differentiation. In contrast, B cells infected with EBV continued to proliferate and retained a blast-like phenotype. Differences in both cytokine production and the expression of cell cycle regulators were identified between the two B-cell populations, which might contribute to the differentiation of the CD40L/IL-4-stimulated B cells and suggest potential mechanisms by which EBV may overcome this. The study has also identified a window of opportunity during which a comparison of isogenic populations of EBV- and mitogen-driven B blasts can be made.

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21

Paul, E. C., J. Hochman, and A. Quaroni. "Conditionally immortalized intestinal epithelial cells: novel approach for study of differentiated enterocytes." American Journal of Physiology-Cell Physiology 265, no. 1 (July 1, 1993): C266—C278. http://dx.doi.org/10.1152/ajpcell.1993.265.1.c266.

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Clonal cell lines have been established from primary fetal rat intestinal epithelial cells by stable transfection with plasmids containing either the simian virus 40 (SV40) large T-antigen gene under the control of the heavy metal inducible metallothionein promoter (pMTWt) or the thermolabile SV40 T-antigen gene under the control of the SV40 early promoter (pZipSVtsa58). pMTWt-transfected cells produced sufficient T-antigen to allow them to proliferate both when the metallothionein promoter was induced and uninduced. No differences were observed in the pattern of intestinal epithelial markers expressed when the cells were cultured in the presence or absence of inducing agent (zinc). In contrast, fetal rat intestinal epithelial cells transfected with pZipSVtsa58 were immortalized conditionally; cells proliferated at 32 degrees C but ceased to proliferate between 48 and 72 h of culture at 39 degrees C. Four of these cell lines were characterized in detail; they showed microvilli and tight junctions as well as dome formation and expressed functional and biochemical markers of intestinal epithelial cells, including keratins 8, 19, and 21, aminopeptidase N, and dipeptidyl peptidase IV. One cell line, 2/4/A1, expressed in addition a low level of lactase and sucrase-isomaltase. The amount and/or activity of some of these markers changed during the switch from the proliferative to the nonproliferative state (switch from culture at 32 to 39 degrees C), resulting in a more differentiated phenotype and mimicking similar changes taking place during intestinal epithelial cell differentiation in vivo.

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22

Tanaka, Y., K. Saito, F. Shirakawa, T. Ota, H. Suzuki, S. Eto, and U. Yamashita. "Production of B cell-stimulating factors by B cells in patients with systemic lupus erythematosus." Journal of Immunology 141, no. 9 (November 1, 1988): 3043–49. http://dx.doi.org/10.4049/jimmunol.141.9.3043.

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Abstract The production of B cell-stimulating factors (BSF) by B cells in patients with systemic lupus erythematosus (SLE) was studied in vitro. B cells from SLE patients markedly proliferated and differentiated into Ig-producing cells by in vitro culture without any stimulation. The culture supernatant of these B cells contained BSF activity that stimulated Staphylococcus aureus Cowan I-treated normal B cells to proliferate and differentiate into Ig-producing cells. By a Percoll gradient density centrifugation, BSF-producing cells were enriched in the higher density fraction, but were reduced in the lower density fraction. The BSF also stimulated the proliferation and the differentiation of SLE B cells. By a Percoll gradient density centrifugation, SLE B cells responsive to the BSF were enriched in the higher density fraction, but were reduced in the lower density fraction. The Mr of the BSF was estimated as about 18,000 Da by Sephacryl S-200 column chromatography. The BSF fraction did not possess IL-2 and IFN activity, but possessed IL-1 activity, which stimulated murine thymocyte proliferative responses. The BSF activity was partially, but not completely, absorbed by an anti-IL-1 alpha antibody. Furthermore, the BSF possessed IL-4 activity, which induced not only the proliferative responses of normal B cells stimulated with B cell mitogens, but also the expression of low affinity Fc epsilon R/CD23 on normal B cells. The BSF also possessed IL-6 activity, which induced the proliferative responses of IL-6-dependent hybridoma cells, MH-60 BSF2. Moreover, human rIL-1, rIL-4, and rIL-6 stimulated SLE B cells. These results suggest that SLE B cells spontaneously produce the BSF such as IL-1 alpha, IL-4, and IL-6 and express their receptors on their surface, and the interaction between the BSF and their receptors stimulates SLE B cells to spontaneously proliferate and differentiate into Ig-producing cells as an autocrine mechanism.

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23

Barnes, D. "AIDS commission bills proliferate." Science 235, no. 4793 (March 6, 1987): 1136. http://dx.doi.org/10.1126/science.3823874.

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24

Fradkin, Eduardo, and Steven A. Kivelson. "Electron Nematic Phases Proliferate." Science 327, no. 5962 (January 7, 2010): 155–56. http://dx.doi.org/10.1126/science.1183464.

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25

Adam, P., C. Schraml, B. Sipos, and F. Fend. "Mesotheliale Proliferate bei Rektumkarzinom." Der Pathologe 35, no. 1 (February 2014): 88–92. http://dx.doi.org/10.1007/s00292-013-1880-0.

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26

DePalma, Angelo. "Protein Expression Systems Proliferate." Genetic Engineering & Biotechnology News 36, no. 2 (January 15, 2016): 1, 20–22. http://dx.doi.org/10.1089/gen.36.02.02.

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27

BARNES, D. M. "AIDS Commission Bills Proliferate." Science 235, no. 4793 (March 6, 1987): 1136b. http://dx.doi.org/10.1126/science.235.4793.1136b.

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28

Brower, Vicki. "Stem cell transformations proliferate." Nature Biotechnology 17, no. 3 (March 1999): 215. http://dx.doi.org/10.1038/6950.

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29

Hollon, Tom. "Gene therapy investigations proliferate." Nature Medicine 6, no. 3 (March 2000): 235. http://dx.doi.org/10.1038/73031.

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30

Nieda, M., T. Juji, S. Imao, and M. Minami. "A role of HLA-DQ molecules of stimulator-adherent cells in the regulation of human autologous mixed lymphocyte reaction." Journal of Immunology 141, no. 9 (November 1, 1988): 2975–79. http://dx.doi.org/10.4049/jimmunol.141.9.2975.

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Abstract In this study, we have found that treatment of stimulator autologous adherent cells with anti-HLA-DQ mAb resulted in markedly enhanced proliferative response of T cells in human autologous mixed lymphocyte reaction system wherein T cells were cultured with autologous adherent cells at near ratio of adherent cells to T cells in peripheral blood, in which T cells minimally proliferate. However, treatment of stimulator-adherent cells with anti-HLA class I, anti-DR and anti-DP mAb had no effect on the proliferative response of T cells under the condition. It was further observed that CD4-enriched cells could significantly proliferate in the presence of autologous adherent cells either untreated or treated with anti-DQ mAb, although treatment of adherent cells with anti-DR mAb blocked proliferative response of CD4-enriched cells. Moreover, the proliferative response of CD4-enriched cells was suppressed by addition of CD8-enriched cells in the presence of untreated adherent cells, whereas the proliferative response of CD4-enriched cells could not be suppressed by CD8-enriched cells when the adherent cells in the culture were treated with anti-DQ mAb. These observations suggest that CD8 T cells are required for suppression of proliferative response of CD4 T cells to HLA-DR molecules on autologous stimulator-adherent cells, and that HLA-DQ molecules on the surface of adherent cells play an important role in the induction of suppression by CD8 T cells.

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31

Gaytán, F., C. Bellido, C. Morales, E. Aguilar, and J. E. Sánchez-Criado. "Evidence for steroidogenic luteal cell hypertrophy and hyperplasia during pregnancy in the rat." Journal of Endocrinology 154, no. 2 (August 1997): 211–17. http://dx.doi.org/10.1677/joe.0.1540211.

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Abstract The proliferative activity of the rat corpus luteum was studied on days 2, 3, 6, 9, 12, 15, 17, 19 and 21 of pregnancy. Proliferating cells were detected by the immunohistochemical demonstration of DNA-incorporated 5-bromodeoxyuridine (BrdU) and by the presence of mitoses. Steroidogenic luteal cells showed two proliferative waves on days 12–15 and on day 21, when relatively abundant BrdU-labeled and mitotic cells were observed. These cells were clearly distinguishable from non-steroidogenic cells by their round nuclei and large polygonal cytoplasm. The proliferative activity on days 12–15 was coincident with an increase in the size of the cells and in progesterone concentrations. On the other hand, the proliferative activity of non-steroidogenic luteal cells (especially endothelial cells of the blood and lymphatic vessels) followed a different pattern. These cells intensely proliferated on days 2–3 of pregnancy and this proliferative activity was significantly higher than that observed in non-pregnant rats on metestrus and diestrus. A new proliferative wave was observed on days 12–15, in association with the increase in the proliferative activity of steroidogenic cells. The presence of both BrdU-labeled and mitotic steroidogenic luteal cells provides evidence that these cells do proliferate and that both hypertrophy and hyperplasia are involved in the increase in the parenchyma of the corpus luteum during pregnancy. Also, the results suggest that different mechanisms are involved in the regulation of the proliferative activity in the corpus luteum at different times during pregnancy. Journal of Endocrinology (1997) 154, 211–217

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32

Goldstein, Michaella, Igal Leibovitch, Shlomo Levin, Yair Alster, Anat Loewenstein, Galina Malkin, and Rafi Korenstein. "Red blood cell membrane mechanical fluctuations in non-proliferative and proliferate diabetic retinopathy." Graefe's Archive for Clinical and Experimental Ophthalmology 242, no. 11 (August 4, 2004): 937–43. http://dx.doi.org/10.1007/s00417-004-0946-3.

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33

Kim, D. K., G. Otten, R. L. Moldwin, D. E. Dunn, G. J. Nau, and F. W. Fitch. "PMA alone induces proliferation of some murine T cell clones but not others." Journal of Immunology 137, no. 9 (November 1, 1986): 2755–60. http://dx.doi.org/10.4049/jimmunol.137.9.2755.

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Abstract The responses of cloned murine T cell lines to the phorbol ester, phorbol myristate acetate (PMA), were investigated. PMA alone was able to stimulate proliferation of some clones but not others. Two Lyt-2+, cloned cytolytic T lymphocyte (CTL) lines proliferated in response to stimulation by PMA alone, but several L3T4+, cloned helper T lymphocyte (HTL) lines did not. In contrast, all clones tested released lymphokines in response to stimulation by the combination of PMA and the calcium ionophore A23187. Moreover, all clones proliferated in response to stimulation by the combination of PMA and A23187. The proliferation of HTL in response to PMA + A23187 could be completely inhibited either by cyclosporine A (CsA) or by PC61.5, a monoclonal antibody directed against the murine IL 2 receptor; however, the proliferation of CTL in response to PMA alone was not affected either by CsA or by PC61.5. These results suggest that of the murine T cell clones tested, HTL proliferate in response to stimulation via an IL 2-dependent, autocrine pathway; in contrast, CTL, in addition to an IL 2-dependent pathway, may possess an additional IL 2-independent pathway of proliferation. CTL that proliferate in response to stimulation by PMA alone may be useful models in the study of T cell proliferation.

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Miescher, S., T. L. Whiteside, S. Carrel, and V. von Fliedner. "Functional properties of tumor-infiltrating and blood lymphocytes in patients with solid tumors: effects of tumor cells and their supernatants on proliferative responses of lymphocytes." Journal of Immunology 136, no. 5 (March 1, 1986): 1899–907. http://dx.doi.org/10.4049/jimmunol.136.5.1899.

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Abstract Tumor-infiltrating lymphocytes (TIL) were obtained from 22 humans with solid tumors. In three cases only, one colon and two lung carcinomas, TIL which contained from 3 to 10% of T cells expressing the interleukin 2 receptor (IL 2R) were obtained, and these proliferated in the presence of exogenous IL 2. In most TIL preparations, however, the T lymphocytes did not express the IL 2R and failed to proliferate in response to IL 2. In contrast, TIL were able to proliferate in response to irradiated allogeneic spleen cells in mixed lymphocyte culture. Proliferative responses of autologous PBL were not inhibited by the addition of TIL. In most tumors, the TIL showed no response or had significantly lower (p less than 0.01) responses to PHA, Con A, and the phorbol ester TPA than did autologous peripheral blood lymphocytes (PBL). A limiting-dilution microculture system which allows clonal growth of every T cell was used to demonstrate decreased responses of the TIL to PHA at a single-cell level. In contrast to normal PBL-T with proliferating frequencies from 0.46 to 1.0, those for T cells in three TIL preparations were zero, 0.005, and 0.01. Normal PBL exposed in vitro to tumor cells or their supernatants lost the ability to respond to mitogens and to clone normally (e.g., proliferating frequency of 0.147 vs 0.863 in control). The TIL isolated from solid tumors resemble normal PBL exposed in vitro to tumor cells or their supernatants in terms of decreased responses to mitogens and poor clonogenicity in the PHA-dependent microculture system. It is possible that tumor cells may inhibit certain functions of the TIL in human solid tumors.

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35

Nixon-Fulton, J. L., W. A. Kuziel, B. Santerse, P. R. Bergstresser, P. W. Tucker, and R. E. Tigelaar. "Thy-1+ epidermal cells in nude mice are distinct from their counterparts in thymus-bearing mice. A study of morphology, function, and T cell receptor expression." Journal of Immunology 141, no. 6 (September 15, 1988): 1897–903. http://dx.doi.org/10.4049/jimmunol.141.6.1897.

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Abstract We have evaluated the morphology, function, and TCR mRNA and DNA profiles of Thy-1+ epidermal cells (EC) derived from athymic (nude) mice. Based on these criteria we demonstrate that Thy-1+ EC in nude mice are predominantly round and angular and located in follicular epithelium, as compared to predominantly dendritic, interfollicular Thy-1+ EC found in normal CBA or BALB/c mice. Functionally, Thy-1+ EC from normal mice proliferate and elaborate IL-2 in response to stimulation by Con A; by contrast, nude Thy-1+ EC fail to proliferate or secrete IL-2 in response to Con A. Nude Thy-1+ EC proliferate markedly in response to low-dose IL-2 alone; Thy-1+ EC from normal mice give only modest proliferative responses to IL-2. Both populations of cells proliferate and elaborate IL-2 in response to PMA and calcium ionophore. Short-term cultured Thy-1+ EC from nude mice resemble Thy-1+ EC from normal animals in that they express no detectable functional TCR-alpha and beta-RNA. Normal Thy-1+ EC express abundant levels of functional RNA for TCR-gamma and delta-chains and for the CD3 delta-chain, whereas nude Thy-1+ EC produce no detectable TCR-delta and no CD3 delta-RNA and only truncated, presumably germ-line TCR-gamma transcripts, as suggested by lack of hybridization with gamma-V region probes and by lack of detectable rearrangements in the gamma-genes. These phenotypic, functional, and genotypic characteristics of Thy-1+ EC from nude mice suggest that these cells are at a very early stage of T cell differentiation.

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Kim, D. K., D. W. Lancki, F. H. Hui, and F. W. Fitch. "Protein kinase C-dependent and -independent mechanisms of cloned murine T cell proliferation. The role of protein kinase C translocation and protein kinase C activity." Journal of Immunology 142, no. 2 (January 15, 1989): 616–22. http://dx.doi.org/10.4049/jimmunol.142.2.616.

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Abstract PMA can induce the proliferation of several CTL clones but not of several Th clones derived and tested in our laboratory. The PMA-stimulated proliferation of our CTL clones (which do not make IL-2 mRNA or protein) occurs independently of IL-2 and is not accompanied by lymphokine release. We now report, however, that protein kinase C (PKC) translocation is induced by PMA in CTL clones as well as in Th clones, which lack a proliferative response to PMA. These results suggest that PKC translocation itself is not a sufficient regulatory mechanism to account for cloned T cell proliferation. Moreover, IL-2 did not induce PKC translocation in a CTL clone, which proliferates when stimulated with IL-2. Thus, PKC translocation may not be necessary for activation of CTL proliferation. Nonetheless, cellular PKC activity appears to be required for the proliferative response of T cell clones after stimulation by PMA/PMA + calcium ionophore (A23187) or by triggering through the TCR: chronic PMA treatment, which depletes intracellular PKC activity, abrogates the proliferative response of T cell clones stimulated by PMA/PMA + A23187 or triggered through the TCR. T cell clones depleted of PKC activity, however, retain the ability to proliferate when challenged with IL-2. Murine T cell clones, therefore, possess PKC-dependent and PKC-independent pathways of proliferation that are not regulated by PKC translocation alone.

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37

Shi En Kim. "Deals proliferate in biotech industry." C&EN Global Enterprise 100, no. 28 (August 15, 2022): 15. http://dx.doi.org/10.1021/cen-10028-buscon3.

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38

Moretti, Michael. "Refractive Laser Sharing Concepts Proliferate." Journal of Refractive Surgery 9, no. 3 (May 1993): 162–64. http://dx.doi.org/10.3928/1081-597x-19930501-03.

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Moretti, Michael. "Refractive Surgery Centers Proliferate Globally." Journal of Refractive Surgery 11, no. 2 (March 1995): 80. http://dx.doi.org/10.3928/1081-597x-19950301-03.

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40

Sivitz, Laura B. "Cells Proliferate in Magnetic Fields." Science News 158, no. 13 (September 23, 2000): 196. http://dx.doi.org/10.2307/3981307.

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41

Glanz, J. "ASTRONOMY:The Coolest Brown Dwarfs Proliferate." Science 284, no. 5420 (June 4, 1999): 1603. http://dx.doi.org/10.1126/science.284.5420.1603.

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42

Raum, Mary. "I DESIRE, THEREFORE I PROLIFERATE." Nonproliferation Review 13, no. 2 (July 2006): 427–31. http://dx.doi.org/10.1080/10736700601012292.

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43

Choi, Kwang-Wook, and Ya-Chieh Hsu. "To Cease or To Proliferate." Cell Adhesion & Migration 1, no. 3 (July 2007): 129–30. http://dx.doi.org/10.4161/cam.1.3.4901.

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44

HELFSTEIN, SCOTT. "Friends Don't Let Friends Proliferate." Political Science Quarterly 125, no. 2 (June 2010): 281–307. http://dx.doi.org/10.1002/j.1538-165x.2010.tb00676.x.

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45

Silva, Orlando de Castro e., and Marina Rodrigues Garcia da Silveira. "To proliferate, not to proliferate or to die. The liver itself decides as needed." Acta Cirurgica Brasileira 29, no. 1 (January 2014): 71–75. http://dx.doi.org/10.1590/s0102-86502014000100011.

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46

Brenchley, Jason M., Nitin J. Karandikar, Michael R. Betts, David R. Ambrozak, Brenna J. Hill, Laura E. Crotty, Joseph P. Casazza, et al. "Expression of CD57 defines replicative senescence and antigen-induced apoptotic death of CD8+ T cells." Blood 101, no. 7 (April 1, 2003): 2711–20. http://dx.doi.org/10.1182/blood-2002-07-2103.

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Virus-specific CD8+ T-cell responses play a pivotal role in limiting viral replication. Alterations in these responses, such as decreased cytolytic function, inappropriate maturation, and limited proliferative ability could reduce their ability to control viral replication. Here, we report on the capacity of HIV-specific CD8+ T cells to secrete cytokines and proliferate in response to HIV antigen stimulation. We find that a large proportion of HIV-specific CD8+ T cells that produce cytokines in response to cognate antigen are unable to divide and die during a 48-hour in vitro culture. This lack of proliferative ability of HIV-specific CD8+ T cells is defined by surface expression of CD57 but not by absence of CD28 or CCR7. This inability to proliferate in response to antigen cannot be overcome by exogenous interleukin-2 (IL-2) or IL-15. Furthermore, CD57 expression on CD8+ T cells, CD4+ T cells, and NK cells is a general marker of proliferative inability, a history of more cell divisions, and short telomeres. We suggest, therefore, that the increase in CD57+ HIV-specific CD8+ T cells results from chronic antigen stimulation that is a hallmark of HIV infection. Thus, our studies define a phenotype associated with replicative senescence in HIV-specific CD8+ T cells, which may have broad implications to other conditions associated with chronic antigenic stimulation.

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47

Mani Tripathi, Kaushalendra. "Returning to the Hallmarks of Cancer: A Brief Review and Revision." Journal of Clinical Research and Reports 9, no. 2 (October 26, 2021): 01–06. http://dx.doi.org/10.31579/2690-1919/200.

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The hallmarks of cancer represent principals and mechanisms on which, different types of cancers function and proliferate, These principals which also include the revised edition include sustained proliferative signaling, Evading growth suppressors , avoiding immune destruction, enabling replicative immortality, tumor promoting inflammation, activating invasion and metastasis, Inducing angiogenesis, genome instability and mutation, resisting cell death, deregulating cellular energetics. This article reviews these hallmarks and suggests any additional hallmark that can be further investigated and integrated into the revised edition , Hanahan and Weinberg’s hallmark of cancer are great pillars of understanding for modern cancer study and are open to modification , making it easily approachable ,critiqued and adds the possibility of additions in the near future. The role of exosomes are discussed with the potential to categorize drug resistance as a separate hallmark to assist us in developing therapeutics that can counter or bypass these mechanisms that assist cancer cells to proliferate even further.

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48

Vivier, E., J. M. Sorrell, M. Ackerly, M. J. Robertson, R. A. Rasmussen, H. Levine, and P. Anderson. "Developmental regulation of a mucinlike glycoprotein selectively expressed on natural killer cells." Journal of Experimental Medicine 178, no. 6 (December 1, 1993): 2023–33. http://dx.doi.org/10.1084/jem.178.6.2023.

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Natural killer (NK) cells are CD3:TCR-, CD16+, CD56+ large granular lymphocytes capable of recognizing and eliminating a variety of virus-infected, malignant, and antibody-coated target cells. Two functionally distinct populations of peripheral blood NK cells can be differentiated by their surface expression of an isoform of the neural cell adhesion molecule (CD56). CD56bright NK cells have the attributes of an undifferentiated cell, in that they proliferate in response to exogenous cytokines, but exert poor cytolytic activity. CD56dim NK cells have the attributes of a more differentiated cell, in that they proliferate poorly in response to exogenous cytokines, but are potent cytolytic effector cells. Here we describe the molecular characterization of a NK cell restricted epitope (PEN5) that is selectively expressed on the functionally differentiated CD56dim NK cells. PEN5+ NK cells proliferate poorly in response to interleukin 2 (IL-2), but are potent cytolytic effectors, whereas PEN5- NK cells proliferate in response to IL-2, but are poor cytolytic effectors. Biochemical and immunochemical analyses reveal the PEN5 epitope to be an unusual sulfated poly-N-lactosamine carbohydrate related to keratan sulfate glycosaminoglycans. Immunoprecipitates prepared using a monoclonal antibody reactive with PEN5 include two polydisperse membrane-bound glycoproteins, PEN5 alpha (120-170 kD) and PEN5 beta (210-245 kD). Enzymatic deglycosylation reduces the apparent molecular weight of both PEN5 isoforms by 80-90%, and classifies PEN5 beta as a mucinlike glycoprotein. The surface expression of the PEN5 epitope is downmodulated by stimuli that induce NK cell proliferation, and it is absent from leukemic NK cells of patients with granular lymphocyte proliferative disorder. Taken together, these results indicate that PEN5 is a developmentally regulated poly-N-lactosamine epitope associated with a mucin-type glycoprotein, whose expression is restricted to the population of nonproliferative NK cells fully committed to cytolytic effector function.

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49

Tedder, T. F., M. D. Cooper, and L. T. Clement. "Human lymphocyte differentiation antigens HB-10 and HB-11. II. Differential production of B cell growth and differentiation factors by distinct helper T cell subpopulations." Journal of Immunology 134, no. 5 (May 1, 1985): 2989–94. http://dx.doi.org/10.4049/jimmunol.134.5.2989.

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Abstract Two monoclonal antibodies (HB-10 and HB-11), which react with human T, B, and NK cells, identify approximately 50% of the Leu-3+ T helper (TH) cells in adult blood. In the present studies, the functional capabilities of the HB-11+ and HB-11-TH cell subpopulations were examined after purification by fluorescence-activated cell sorting. Both subpopulations proliferated in response to PHA, Con A, PWM, and OKT-3 antibodies. The HB-11+ TH cells gave a minimal proliferative response to soluble tetanus toxoid antigen, whereas HB-11-TH cells responded well. After mitogen activation, both HB-11+ and HB-11-TH cells and to produce soluble factors which induce large B cells to proliferate. However, PWM-stimulated HB-11+TH cells were incapable of inducing B cells to differentiate into antibody-secreting plasma cells, whereas HB-11-TH cells were efficient in this regard. The results suggest that the HB-11 antigen is expressed on a subpopulation of virgin TH cells that can produce B cell growth factors but are deficient in the ability to produce B cell differentiation factors.

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50

Krowka, J., D. Stites, R. Debs, C. Larsen, J. Fedor, E. Brunette, and N. Düzgünes. "Lymphocyte proliferative responses to soluble and liposome-conjugated envelope peptides of HIV-1." Journal of Immunology 144, no. 7 (April 1, 1990): 2535–40. http://dx.doi.org/10.4049/jimmunol.144.7.2535.

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Abstract The proliferation of lymphocytes from HIV-seronegative (HIV Ab-) and seropositive (HIV Ab+) individuals in response to two synthetic peptide epitopes of HIV envelope glycoproteins (ENVgp) was evaluated as an index of cell-mediated immunity in infected individuals. All HIV Ab- and most HIV Ab+ individuals' lymphocytes failed to proliferate in primary cultures in response to the two soluble HIV ENVgp peptides, ENVP346 and ENVP466 even in the presence of rIL-2. After stimulation with liposome-conjugates of ENVP346 or ENVP466 and soluble rIL-2, however, CD4 lymphocytes from some HIV Ab+ individuals were able to proliferate. Significantly higher frequencies of rIL-2-augmented proliferative responses to liposome-conjugated ENVP346 or ENVP466 were observed in HIV Ab+ asymptomatic individuals as compared to patients with AIDS-related conditions or AIDS. These studies indicate that the conjugation of HIV peptides or proteins to liposomes and stimulation with rIL-2 may enhance cell-mediated responses to these peptides.

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