Cell lines Jurkat

Example using a suspension cell line (Jurkat T-leukemia cell) (see Notes 3 and 4). 

Fiorentini C, Chow SC, Mastrantonio P, et al. (1992) Clostridium difficile toxin A induces multinucleation in the human leukemic T cell line JURKAT. In Eur. J. Cell Biol. 57 292-297. 

CD95-induced apoptosis in the human T-cell line Jurkat ean be readily inhibited by bloeking aSMase (A.Billich, unpublished data). 

Purification and Biochemical Properties of IL-2. Early approaches to the purification of IL-2 involved classical preparative and chromatographic methods coupled with a search for T cell lines which did not produce other factors (such as colony stimulating factor, B cell growth factors, lymphocyte activating factor). IL-2 from the cloned human leukemia T-cell line JURKAT has been used for purification and... 

Human leukemia cell lines Jurkat pharmacologic inhibitors DNA minor groove binding methylsulfonateester lexitropsin [MeOSO(2)(CH(2))(2)-J 58... 

Raubenheimer reported the anti-cancer activity of compound 34 (Figure 4.9).This complex was tested on human cervical epithelioid carcinoma cell line HeLa, human colon adenocarcinoma cell line CoLo 320 DM, leukaemia cell line Jurkat, and breast cancer cell line MCF-7. IC50 values determined by the MTT assay showed human lymphocytes were less sensitive than the cancer cells tested, indicating some selectivity for the cancer cells. 

Journet A et al. Towards a human repertoire of monocytic lysosomal proteins. Electrophoresis 2000 21 3411-3419. Soskic V et al. Functional proteomics analysis of signal transduction pathways of the platelet-derived growth factor beta receptor. Biochemistry 1999 38 1757-1764. Thiede B et al. A two dimensional electrophoresis database of a human Jurkat T-cell line. Electrophoresis 2000 21 2713-2720. 

As was the case for most other cytokines, medical appraisal/use of IL-2 was initially impractical due to the minute quantities in which it is normally produced. Some transformed cell lines, most notably the Jurkat leukaemia cell line, produces IL-2 in increased quantities, and much of the IL-2 used for initial characterization studies was obtained from this source. Large-scale IL-2 production was made possible by recombinant DNA technologies. Although the IL-2 gene/cDNA has now been expressed in a wide variety of host systems, it was initially expressed in E. coli, and most products being clinically evaluated are obtained from that source. As mentioned previously, the absence of glycosylation on the recombinant product does not alter its biological activity. 

This may be complemented with ex vivo gene profiling of PBMC from patients on immunosuppressive drugs. Finally, instead of using fresh human PBMC and rodent splenocytes, cell lines such as the human Jurkat T-cell line and the mouse EL4 thymoma cell line can be used. 

The dimers were studied more closely in HL-60 leukaemia and Jurkat cell lines, and it was found that they have activities comparable to the clinically nsed anticancer drng doxorubicin. In terms of general toxicity to normal cells, it was observed that dimers 115 and 116 were not toxic to lymphocytes at doses approaching 100 p,M. In preliminary studies, apoptotic cell death was observed on exposnre to these componnds and further studies are ongoing to elucidate the underlying mechanism of apoptosis. For purposes of comparison, the corresponding phosphate ester monomers 117 and 118 were prepared and proved to have no antitumour activity in the cell lines examined. This result is important, because it rules out any role of the phosphate ester functionality in mediating the observed cytotoxic effects and emphasizes the necessity for a bivalent unit. 

Parallel to our group, a few other researchers also performed significant studies on anticancer (3-lactams. For example, (3-lactam derivatives (Fig. 2) induced DNA damage, inhibited DNA replication, and activated the apoptotic death program in human leukemic Jurkat T cells in a time and concentration-dependent manner. Importantly, (3-lactam 69 also inhibited proliferation and induced apoptosis in other human solid tumor cell lines (breast, prostate, and head-and-neck). It was believed that induction of apoptosis by 69 is associated with activation of p38 mitogen-activated protein (MAP) kinase, release of mitochondrial cytochrome c, and activation of the caspases. It was reported that apoptosis is blocked by a specific inhibitor to p38 kinase, implicating p38 MAP kinase as the major factor in (3-lactam-induced apoptosis [154]. This study was very significant. 

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