Viewing negative mentions of positive regulation of IL2 (H. sapiens) in NK cells

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Darko et al. (1988)interleukin-2natural killer cellsPercent of total lymphocytes labeled as all T lymphocytes, all B lymphocytes, and natural killer cells did not differ in the two groups, nor did mitogen-induced interleukin-2 production.
Santos et al. (1996)interleukin 2NK cellThe reason for this is unknown; however, it was not due to an increase in the percentage of NK cells, nor to an increase in interleukin 2 (IL-2) receptor expression, nor to IL-2 production. beta-carotene may be acting directly on one or more of the lytic stages of NK cell cytotoxicity, or on NK cell activity-enhancing cytokines other than IL-2, such as IL-12.
Ortaldo et al. (1995)IL-2NK cellsPeripheral NK cells were examined for ligand-induced death using antibodies to surface moieties (CD2, CD3, CD8, CD16, CD56), with and without prior activation of IL-2.
Melder and Jain (1992)IL-2NK cellsReintroduction of IL-2 for 24 h to a culture of NK cells depleted of IL-2 for 48 h did not restore the cells to the pre-depletion level of rigidity.
Gonzalez-Amaro et al. (1988)IL-2NK cellsThis apparent normalcy was found to be maintained by few NK cells with high recycling activity that could not be increased further with IL-2.
Aoki and Fukuchi (1987)interleukin-2natural killer cellThese results indicate that the mechanism of activation of human natural killer cell activity by medullasin is not mediated by the induction of interferons or interleukin-2.
Kawakami et al. (1989)IL-2null cellsIn contrast to unstimulated cells, IL-4 alone induced marked cell proliferation and LAK activity as well as Leu-19+ cells from in vitro IL-2 preactivated PBMC or null cells, and did not inhibit IL-2 induced cell proliferation, LAK activity, Leu-19+ cells and IL-2R(p55) expression, but rather augmented them with low doses of IL-2.
Zambello et al. (1994)interleukin-2natural killer cellsIndependent expression of p55 and p75 interleukin-2 receptors (IL-2R) during intravenous or subcutaneous administration of recombinant interleukin-2 (rIL-2) by T-lymphocytes and natural killer cells.
Yu et al. (2000)IL-2NK cellsThis data indicate that p38 MAPK activation was not required for IL-2 to activate NK cells for the four functions examined.