LAUSR

In the last two decades, “Immunometabolism” has emerged as a continuously increasing area of research with significant impact on biomedicine [1, 2]. The term immunometabolism defines the interface between immunology and metabolism. The crosstalk between these two major research directions has multiple facets. For instance, immune cells present in the adipose tissue or liver regulate tissue homeostasis and metabolic functions, such as lipolysis or the actions of insulin [3–6]. Intake of nutrients, such as sugars, fat, or proteins, and the metabolism thereof may modulate immune responses [4]. Furthermore, the presence of chronic metabolic inflammation, also called “metaflammation” is a central hallmark of metabolic disorders [7]. Metabolic inflammation, orchestrated by cellular and molecular components of the immune response and affecting the adipose tissue, the liver, or the pancreas, contributes to pathogenesis and progression of conditions associated with obesity, such as type 2 diabetes or non-alcoholic fatty liver disease [1, 3, 5, 7]. For instance, both accumulation and activation of macrophages in the adipose tissue and the liver in obesity are implicated in the progression of metabolic disorders [3, 5]. Interestingly, the function of macrophages in the adipose tissue and liver in obesity is regulated by adaptations of their metabolism, triggered by the lipid-rich tissue environment [3]. Accordingly, the obese adipose tissue and liver are characterized by the enrichment of a macrophage subpopulation with a lipid metabolism-related signature, designated “lipid-associated macrophages,” as recently identified by analysis at the single-cell level [8, 9]. An important additional layer of the crosstalk between immunology and metabolism is illustrated by the fact that cellular metabolism is a central regulator of the function and activation of immune cells [3, 10]. Distinct activation states of innate immune cells, especially macrophages, are associated with different cellular metabolic states; hence, cell metabolic adaptations facilitate macrophage phenotype and plasticity [3, 10]. Metabolic reprogramming of innate immune cells is also an essential component of innate immune memory, also designated trained immunity, which defines that certain stimuli may promote unspe-