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Illegal Beings: Human Clones
A deletion mutant of Pseudomonas exotoxin-A fused to recombinant human interleukin-9 (rhIL-9-ETA') shows specific cytotoxicity against IL-9-receptor-expressing cell
Klimka A, Barth S, Drillich S, Wels W, van Snick J, Renauld JC, Tesch H, Bohlen H, Diehl V, Engert ACytokines Mol Ther. 1996 Sep;2(3):139-46..
Medizinische Universitatsklinik I, Cologne, Germany.
The receptor for human interleukin-9 (hIL-9) might be a target for selective immunotherapy. It is expressed on a variety of malignant cells, including Hodgkin's lymphoma, non-Hodgkin lymphoma and acute myeloid leukemia (AML). We therefore constructed a new chimeric toxin by fusing hIL-9-cDNA to modified Pseudomonas aeruginosa exotoxin A (ETA'). The binding properties of the new recombinant protein, rhIL-9-ETA', were assessed on different cell lines expressing the hIL-9 receptor. The antitumor potency of rhIL-9-ETA' was evaluated against the Hodgkin-derived cell lines L540Cy, KM-H2 and L1236, the Burkitt lymphoma cell line Daudi, the erythroleukemia cell line K562, and the mastocytoma cell line P815-hIL9R, transfected with hIL-9 receptor cDNA. Recombinant hIL-9-ETA' exhibited potent specific cytotoxic effects against P815-hIL9R, K562 and L1236 cells, inhibiting protein synthesis by 50% (IC50) at concentrations of 0.05, 0.58 and 3 micrograms/ml respectively. The cytotoxic effect was abrogated after addition of polyclonal antibodies against the human IL-9. rhIL-9-ETA' might be of potential use against hIL-9R-expressing malignancies.
This Message is being posted for educational purposes, as well as for comment and criticism, by the visitors to the HumanCloning.org Foundation website (http://www.humancloning.org ).
Disclaimer: This abstract is being posted for educational purposes, as well as for comment and criticism, by the visitors to the Human Cloning Foundation website (www.HumanCloning.org ). This abstract is representative of a larger article that is indexed on Medline.
The Human Cloning Foundation was established February, 1988. .
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