AI Article Synopsis
- - Immune cells adjust their metabolic processes when facing fungal infections, shifting from glycolysis to the serine synthesis pathway (SSP) and one-carbon metabolism.
- - The interaction between spleen tyrosine kinase (SYK) and phosphoglycerate dehydrogenase (PHGDH) is key, as SYK phosphorylation leads to the activation of signaling that boosts pro-inflammatory cytokine production.
- - This study highlights how amino acid metabolism, epigenetic changes, and C-type lectin receptor (CLR) signaling work together during fungal infections, enhancing our understanding of immune responses.
Article Abstract
Immune cells modify their metabolic pathways in response to fungal infections. Nevertheless, the biochemical underpinnings need to be better understood. This study reports that fungal infection drives a switch from glycolysis to the serine synthesis pathway (SSP) and one-carbon metabolism by inducing the interaction of spleen tyrosine kinase (SYK) and phosphoglycerate dehydrogenase (PHGDH). As a result, PHGDH promotes SYK phosphorylation, leading to the recruitment of SYK to C-type lectin receptors (CLRs). The CLR/SYK complex initiates signaling cascades that lead to transcription factor activation and pro-inflammatory cytokine production. SYK activates SSP and one-carbon metabolism by inducing PHGDH activity. Then, one-carbon metabolism supports S-adenosylmethionine and histone H3 lysine 36 trimethylation to drive the production of pro-inflammatory cytokines and chemokines. These findings reveal the crosstalk between amino acid metabolism, epigenetic modification, and CLR signaling during fungal infection.
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Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11618577 | PMC |
| http://dx.doi.org/10.1038/s41418-024-01374-7 | DOI Listing |
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