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Central to this complexity is a dysregulated host response, driven by hyperinflammation, immune suppression, and profound mitochondrial and metabolic dysfunction

For example, patients often have lower levels of anti-inflammatory bacteria such as Faecalibacterium and higher proportions of pro-inflammatory species, which may contribute to systemic inflammation and symptom severity (Knig et al., 2021

RAS and RHO families of GTPases directly regulate distinct phosphoinositide 3-kinase isoforms