Table 1 Recent evidence and potential mechanisms of IL-38 in infections
From: Novel insights into the role of anti-inflammatory IL-38 in immunity against infection
Pathogenic diseases | Models | Expression and regulation of IL-38 | References | |
|---|---|---|---|---|
Influenza | Human study and animal model | Increased IL-38 levels in patients with influenza, returned to baseline once recovered. | IL-38 counteracts the proinflammatory effects of IL-36α. | Gao et al. [4] |
COVID-19 | Human study and animal model | Increased IL-38 levels in patients with SARS-CoV-2, negatively correlated with disease severity. | ||
Human study | IL-38 levels were not influenced by COVID-19, disease severity, sex, age, or chronic disease, while obese people showed lower IL-38 levels. These parameters have concurrent impacts on IL-38 levels. | Al-Bassam et al. [5] | ||
Chronic hepatitis B | Human study | Decreased levels of IL-38 in HBV infection patients, and IL-38 was assumed to be pathogenic in the case of HBV infection. | Alaaraji [6] | |
Human study | Increased IL-38 levels in chronic hepatitis B patients, and IL-38 served as a biomarker of liver damage and positive virological response to antiviral treatment. | Wang et al. [7] | ||
HCV infection | Human study | Higher IL-38 levels in treated HCV infection patients and healthy individuals than in pretreated patients; patients with higher IL-38 levels showed reduced liver injury. | Fazeli et al. [8] | |
Fungal infection | Cell model | IL-38 inhibited C. albicans-induced Th17 cytokine production. | Van de Veerdonk et al. [2] | |
Sepsis | Human study and animal model | Elevated IL-38 levels correlated negatively with IL-6 and TNF-α levels in sepsis; exogenous IL-38 improved survival of septic mice. | Xu et al. [11] | |
Animal model | Increased IL-38 levels were produced by CD4 + CD25 + Treg cells and, in turn, increased survival of septic mice by enhancing production of IL-10, TGF-β1 and Tregs. | Ge et al. [12] | ||
Animal model | IL-38 promoted M2 macrophage polarization, inhibited macrophage apoptosis, and suppressed NLRP3 inflammasome activation in macrophages. | Ge et al. [13] | ||
ARDS | Human study, animal model and cell model | Elevated IL-38 levels in ARDS; IL-38 protected from ARDS by inhibiting the differentiation of Th17 cells. | Chai et al. [14] | |
Trained immunity | Human study, animal model and cell model | IL-38 prevented the proinflammatory epigenetic reprogramming in the subsequent response to secondary stimulation by LPS. SNP rs5896312 affected both plasma IL-38 levels and the inducibility of trained immunity in monocytes. | de Graaf et al. [15] | |
