Table 1 List of the main articles evaluating how IL-33 is influenced by and influence gene expression
From: IL-33 genetics and epigenetics in immune-related diseases
Reference | Disease | Tissue | Genetic pathways | Effects |
|---|---|---|---|---|
[16] | - | CNS / microglia | Apigenin and luteolin inhibit Iba-1 | They act on IL-31 and NF-κB by reducing IL-33 production |
[17] | Ischemia-reperfusion, renal injury | Kidneys | The chromatin remodeling protein BRG1 | It regulates the transcription of IL-33 |
[18] | MS | PBMC cells | HDAC3 | It acts by transcriptional repressor of IL-33 |
[19] | MS | CNS | DND1, PET100, GPR160, LPAR6, and SERTAD3 correlate with IL-33 | These genes, but not IL-33, are involved in DNA repair or mitochondrial function and mRNA splicing pathways. |
[20] | Infection of Mesocestoides corti and Nippostrongylus brasiliensis | Bone marrow (eosinophil) | Dusp5 | IL-33-activated Dusp5/ eosinophils had improved cellular ERK1/2 activation and BCL-XL expression resulting in higher eosinophil survival |
[21] | Atherosclerotic and inflammatory diseases | HUVECs cells | IL-8 gene | IL-33 induces IL-8 expression through the activation of JNK/c-Jun/AP-1 pathway causing inflammatory syndromes |
[22] | Allergic asthma | Lung | siRNA blockade of Rip2 | Therefore, it blocks the expression of IL-33 ameliorating inflammation |
[23] | Acute lung injury | Lung | NLRP3 silencing | Reduce IL-33 expression |
[24] | Alzheimer’s disease | Brain/microglia | IL-33-provoked remodeling of chromatin accessibility and PU0.1 transcription factor binding | Modify microglial epigenetic and transcriptomic profiles resulting in Alzheimer amelioration |
[25] | Allergic diseases | Lung | Trimethylated lysine 27 of histone H3 at promoter regions of IL-33 | Down-regulation of IL-33 |
[26] | Cardiovascular diseases | Heart | PKCβ/JNK | IL-33 inhibits apoptosis |