Figure 3.

Novel insights into Treg modulation in sepsis. During sepsis, metabolites such as lactic acid and adenosine, along with inflammation-related factors like CIRP, are produced systemically as a result of inflammatory responses and tissue injury. These elements intricately affect Treg metabolism, their differentiation process, and the expression of surface inhibitory molecules via various molecular pathways. Furthermore, immune cells present in the septic environment—particularly neutrophils, macrophages, and DCs—play a role in modulating Treg differentiation and function by releasing immunoregulatory cytokines such as IL-10 and TGF-β. CIRP cold-inducible RNA-binding protein, IL-10 interleukin-10, TGF-β transforming growth factor-beta