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KMID : 0360319890210020328
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Journal of Korean Cancer Research Association
1989 Volume.21 No. 2 p.328 ~ p.338
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Comparative Study on In Vitro Biological Activity of Human Natural and Recombinant Interleukin 2 (IL2)
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남상윤/Nam, Sang Yun
박재경/함경수/최규철/하윤문/한문희/이연태/Park, Jai Kyung/Hahm, Kyung-Soo/Choeh, Kyuchul/Ha, Youn Mun/Han, Moon Hee/Lee, Yun Tai
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Abstract
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Recently some authers of us have described successful production of human recombinant interleukin 2 (rIL 2). In concideration of future application in vitro and in vivo of rIL 2, this study was carried out in an attempt to confirm the biological activities of the rIL 2 and compare with those of human natural IL 2 (nIL 2) on a per unit basis.
The two IL 2 preparations induced CTLL-2 cell proliferation at the equivalent level. This result showed that nIL 2 and rIL 2 activity could be evaluated with same assay system.
Dose response of IL 2 in lymphokine-activated killer (LAK) cell induction was also similar. Greatest activity of LAK cells was induced with 500~1,000 U/ml (target, Raji) or 100~1,000 U/ml (target, K -562) of IL 2, and the activity decreases over 5,000 U/ml of rIL 2. In LAK cell induction kinetics, peak activity was seen after 4 (targe, Raji) to 5 day-culture (target, K-562) with rIL 2 and nIL 2. Thereafter, activity of LAK cells generated with nIL 2 declind whereas it was sustained (target, K-562) or enhanced successively (target, Raji) with rIL 2. Similar results were also seen in a prolonged activation of LAK cells for 9~14 days. Augmentation effect of IL 2 on natural killer cell activity by 24 hr-treatment was comparable between nIL 2 and rIL 2 except that higher peak activity was observed with rIL 2 than with nIL 2. These data suggested that nIL 2 might be different from rIL 2 in some biological activities, although we cannot exclusively rule out the possibility that some other related lymphokines are present in nIL 2 preparation.
Subsequent experiments for elucidation of the mechanisms for the differential activities demonstrated that the functional differences of the two IL 2 preparations observed above were due to neither lability nor poor IFN induction of nIL 2. Thus, it was assumed that activation or proliferation of any other cell populations than LAK effector or precursor cells, e.g., suppressor cells, might be involved in the mechanism.
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