Figure 2
Figure 2. Transudative pleural fluid and nonmalignant ascites inhibit rituximab-induced NK cell CD16 down-modulation and CD54 up-regulation. PBMCs and Raji cells were mixed at a 1:1 ratio for 20 hours in the presence or absence of 50% pleural fluid or ascites with various concentrations of rituximab. NK cell–surface marker expression was determined by flow cytometry with gating on CD3−, CD56+ lymphocytes. (A) NK cell CD16, expressed as median fluorescence, in the absence and presence of pleural fluid or ascites fluid (n = 3 samples per group). (B) NK cell CD54, expressed as a percentage of CD54 bright, in the absence and presence of pleural fluid or ascites fluid (n = 3 samples per group). Error bars represent SD of the mean.

Transudative pleural fluid and nonmalignant ascites inhibit rituximab-induced NK cell CD16 down-modulation and CD54 up-regulation. PBMCs and Raji cells were mixed at a 1:1 ratio for 20 hours in the presence or absence of 50% pleural fluid or ascites with various concentrations of rituximab. NK cell–surface marker expression was determined by flow cytometry with gating on CD3, CD56+ lymphocytes. (A) NK cell CD16, expressed as median fluorescence, in the absence and presence of pleural fluid or ascites fluid (n = 3 samples per group). (B) NK cell CD54, expressed as a percentage of CD54 bright, in the absence and presence of pleural fluid or ascites fluid (n = 3 samples per group). Error bars represent SD of the mean.

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