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CPT2 mediated fatty acid oxidation is dispensable for humoral immunity.

Meilu LiXian ZhouXingxing ZhuYanfeng LiTaro HitosugiYuzhen LiHu Zeng
Published in: bioRxiv : the preprint server for biology (2024)
B cell activation is accompanied by dynamic metabolic reprogramming, supported by a multitude of nutrients that include glucose, amino acids and fatty acids. While several studies have indicated that fatty acid mitochondrial oxidation is critical for immune cell functions, contradictory findings have been reported. Carnitine palmitoyltransferase II (CPT2) is a critical enzyme for long-chain fatty acid oxidation in mitochondria. Here, we test the requirement of CPT2 for humoral immunity using a mouse model with a lymphocyte specific deletion of CPT2. Stable 13 C isotope tracing reveals highly reduced fatty acid-derived citrate production in CPT2 deficient B cells. Yet, CPT2 deficiency has no significant impact on B cell development, B cell activation, germinal center formation, and antibody production upon either thymus-dependent or -independent antigen challenges. Together, our findings indicate that CPT2 mediated fatty acid oxidation is dispensable for humoral immunity, highlighting the metabolic flexibility of lymphocytes.
Keyphrases
  • fatty acid
  • immune response
  • hydrogen peroxide
  • mouse model
  • oxidative stress
  • amino acid
  • heavy metals
  • cell death
  • blood pressure
  • electron transfer
  • risk assessment
  • blood glucose