Back

Linoleoyl-lysophosphatidylcholine suppresses immune-related adverse events due to immune checkpoint blockade

Mathews, I. T.; Saminathan, P.; Henglin, M.; Liu, M.; Nadig, N.; Fang, C.; Mercader, K.; Chee, S. J.; Campbell, A. M.; Patel, A. A.; Tiwari, S.; Watrous, J. D.; Ramesh, K.; Dicker, M.; Dao, K.; Meyer, M. A.; Jousilahti, P.; Havulinna, A. S.; Niiranen, T.; Salomaa, V.; Joosten, L. A.; Netea, M. G.; Zheng, P.; Kronenberg, M.; Patel, S. P.; Gutkind, J. S.; Ottensmeier, C.; Long, T.; Kaech, S. M.; Hedrick, C. C.; Cheng, S.; Jain, M.; Sharma, S.

2024-08-08 oncology
10.1101/2024.08.07.24310974 medRxiv
Show abstract

Immune related adverse events (irAEs) after immune checkpoint blockade (ICB) therapy occur in a significant proportion of cancer patients. To date, the circulating mediators of ICB-irAEs remain poorly understood. Using non-targeted mass spectrometry, here we identify the circulating bio-active lipid linoleoyl-lysophosphatidylcholine (LPC 18:2) as a modulator of ICB-irAEs. In three independent human studies of ICB treatment for solid tumor, loss of circulating LPC 18:2 preceded the development of severe irAEs across multiple organ systems. In both healthy humans and severe ICB-irAE patients, low LPC 18:2 was found to correlate with high blood neutrophilia. Reduced LPC 18:2 biosynthesis was confirmed in preclinical ICB-irAE models, and LPC 18:2 supplementation in vivo suppressed neutrophilia and tissue inflammation without impacting ICB anti-tumor response. Results indicate that circulating LPC 18:2 suppresses human ICB-irAEs, and LPC 18:2 supplementation may improve ICB outcomes by preventing severe inflammation while maintaining anti-tumor immunity.

Matching journals

The top 2 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.