Fig. 9.
Fig. 9. hrIL-6M derived from. / E coli inhibit hrIL-6D–prevented B-CLL apoptosis. (A) hrIL-6 derived from E coli was filtered through a Sephacryl G-200 column, and fractions were analyzed for IL-6 content by ELISA. The Mr standards are indicated by arrows. (B) B-CLL cells were cultured in the presence of various concentrations of hrIL-6D (■) or hrIL-6M (●) derived fromE coli. hrIL-6D exhibited saturation of B-CLL survival at 10 ng/mL. Results are expressed relative to the percentage of apoptosis observed in the CM. (C) In the same experiment, inhibition of hrIL-6D–prevented B-CLL apoptosis by hrIL-6M was measured by mixing varying concentrations of hrIL-6M with an optimal concentration (10 ng/mL) of hrIL-6D. Similar results were observed in 2 additional experiments. Percentages of apoptotic cells were measured in a 48-hour assay.

hrIL-6M derived from

E coli inhibit hrIL-6D–prevented B-CLL apoptosis. (A) hrIL-6 derived from E coli was filtered through a Sephacryl G-200 column, and fractions were analyzed for IL-6 content by ELISA. The Mr standards are indicated by arrows. (B) B-CLL cells were cultured in the presence of various concentrations of hrIL-6D (■) or hrIL-6M (●) derived fromE coli. hrIL-6D exhibited saturation of B-CLL survival at 10 ng/mL. Results are expressed relative to the percentage of apoptosis observed in the CM. (C) In the same experiment, inhibition of hrIL-6D–prevented B-CLL apoptosis by hrIL-6M was measured by mixing varying concentrations of hrIL-6M with an optimal concentration (10 ng/mL) of hrIL-6D. Similar results were observed in 2 additional experiments. Percentages of apoptotic cells were measured in a 48-hour assay.

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