ArticleScientific reports2024
Downhill running does not alter blood C1q availability or complement-dependent cytotoxicity of therapeutic monoclonal antibodies against haematological cancer cell lines in vitro.
Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Characterising how a single bout of exercise in people with myeloma affects clonal plasma cell and immune effector cell frequency in blood, and daratumumab efficacyBrain, behavior, & immunity - health · 2024Article
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14 authors.
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Abstract
Complement-dependent cytotoxicity (CDC) is a primary mechanism-of-action of monoclonal antibody (mAb) immunotherapies used to treat haematological cancers, including rituximab and daratumumab. However, mAb efficacy may be limited by reduced bioavailability of complement C1q - which activates the complement classical pathway following interactions with mAb-opsonised target cells. C1q is secreted by phagocytes upon recruitment to sites of muscle damage to facilitate muscular repair, hence we hypothesised that muscle damaging exercise may increase C1q 'spill-over' into blood. Additionally, other complement proteins (e.g., C1s) have been reported to increase following ultra-endurance and resistance exercise. Taken together, we hypothesised that muscle damaging exercise could be harnessed to enhance mAb-mediated CDC. In this study, n = 8 healthy males (28 ± 5-years) completed two 45-minute treadmill running protocols: (1) a flat running protocol at a speed 15% above anaerobic threshold, and (2) a downhill running protocol (- 10% slope) at the same speed. Blood samples were collected before, immediately after, and 1-hour, 24-hours, 2-days, and 4-days after exercise. Isolated serum was assessed for C1q by ELISA, and used to measure mAb (rituximab, daratumumab) mediated CDC against two haematological cancer cell lines (Raji, RPMI-8226) in vitro. Isolated plasma was assessed for markers of inflammation (C-reactive protein [CRP]), and muscle damage (creatine kinase [CK]) by turbidimetry. C1q and CDC activity were not different between running protocols and did not change over time (p > 0.05). Significantly greater perceived muscle soreness (p < 0.001) and fluctuations observed from baseline to 24-hours post-exercise in the downhill running trial in CK (+ 171%) and CRP (+ 66%) suggests some degree of muscle damage was present. It is possible that any increase in C1q post-exercise may have been masked by the increase and subsequent interaction with CRP, which utilises C1q to facilitate muscular repair. This is the first study to investigate whether exercise can increase circulating C1q and improve mAb-mediated CDC and our findings show that downhill running exercise does not increase circulating C1q nor improve CDC in vitro.
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