Natalie Eaton
Griffith University, Australia
Title: Rituximab impedes natural killer cell function in chronic fatigue syndrome/myalgic encephalomyelitis patients: A pilot In vitro investigation
Biography
Biography: Natalie Eaton
Abstract
Rituximab impedes natural killer (NK) cells function in Chronic Fatigue Syndrome/Myalgic Encephalomyelitis (CFS/ME) patients: A pilot in vitro investigation outlines the toxicological effect Rituximab has on the cytotoxic activity of NK cells isolated from CFS/ME patients. CFS/ME is a multifactorial disorder commonly characterised by reduced NK cell cytotoxicity. A total of 8 CFS/ME patients (48.63 ± 15.69 years) and 9 non-fatigued controls (NFC) (37.56 ± 11.06 years) were included using the Fukuda case definition. Apoptotic function, lytic proteins (granzyme A and granzyme B) and degranulation markers (CD107a and CD107b) were measured on NK cells using flow cytometric analysis prior to and following overnight incubation with Rituximab at 10µg/ml and 100µg/ml. We reported a significant reduction in NK cell lysis of target K562 cells in CFS/ME patients compared to NFC following incubation with 100µg/ml of Rituximab (p<0.05). Conversely, no significant difference was reported for NFC following incubation with Rituximab. There was also a significant decrease in granzyme B in CFS/ME patients compared to NFC with 100µg/ml of Rituximab prior to K562 cells stimulation (p<0.05). Moreover, a significant increase in CD107a (p<0.05) and CD107b (p<0.01) expression was observed in NFC after stimulation with K562 cells prior to incubation with Rituximab. There was a significant increase in CD107b expression in CFS/ME patients before and after overnight incubation with 100µg/ml of Rituximab prior to K562 cells stimulation (p<0.01). This study showed that Rituximab can have significant impairment on NK cell activity and finally the toxicological effects may worsen patients’ symptoms..