Figure 3
Figure 3. Inhibitory effect of transudative pleural fluid and nonmalignant ascites is dose dependent and abrogated by heat inactivation. PBMCs and Raji cells were mixed at a 1:1 ratio for 20 hours in various concentrations of pleural fluid, ascites, or heat-inactivated samples in the presence of 5 μg/mL rituximab. NK cell–surface marker expression was determined by using flow cytometry with gating on CD3−, CD56+ lymphocytes. (A) NK cell CD16, expressed as median fluorescence, after incubation with various concentrations of pleural fluid, ascites, or heat-inactivated samples (n = 3 samples per group). (B) NK cell CD54, expressed as a percentage of CD54 bright, after incubation with various concentrations of pleural fluid, ascites, or heat-inactivated samples (n = 3 samples per group). Error bars represent SD of the mean.

Inhibitory effect of transudative pleural fluid and nonmalignant ascites is dose dependent and abrogated by heat inactivation. PBMCs and Raji cells were mixed at a 1:1 ratio for 20 hours in various concentrations of pleural fluid, ascites, or heat-inactivated samples in the presence of 5 μg/mL rituximab. NK cell–surface marker expression was determined by using flow cytometry with gating on CD3, CD56+ lymphocytes. (A) NK cell CD16, expressed as median fluorescence, after incubation with various concentrations of pleural fluid, ascites, or heat-inactivated samples (n = 3 samples per group). (B) NK cell CD54, expressed as a percentage of CD54 bright, after incubation with various concentrations of pleural fluid, ascites, or heat-inactivated samples (n = 3 samples per group). Error bars represent SD of the mean.

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