| China 2020; Hou et al. [11] |
CRISPR/Cas9 human IL-37b knock-in mice |
IL-37b impeded the in vitro production of pro-inflammatory cytokines IL-6 and TNF-α, and chemokines CXCL8, CCL2, and CCL5. Il-37 enhanced LC3 conversion, an indicator of autophagy, and decreased p62, an indicator of autophagy flux, and piled inside cells when autophagy was inhibited, and the other way around. IL-37b substantially boosted Foxp3+ regulatory T cells (Treg) and IL-10, and reduced eosinophil infiltration in ear lesions. IL-37b repaired the disrupted gut microbiota diversity by modulating the intestinal metabolite-mediated autophagy mechanism.
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| China 2021; Hou et al. [12] |
CRISPR/Cas9 human IL-37b knock-in mice or mice with direct treatment with human IL-37b antibody |
IL-37b reduced thymic stromal lymphopoietin (TSLP) expression as well as the expression of TSLP receptor and basophil activation marker CD203c on basophils. IL-37 reduced the release of IL-4. Upon direct treatment with a human IL-37b antibody, AD symptoms such as ear swelling and itching were alleviated.
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| United States of America 2019; Guttman-Yassky et al. [13] |
51 children (less than 5 years); 21 with moderate-to-severe AD with less than 6 months of disease duration; 30 did not have AD; RNA extracted from tape strips; quantitative RT-PCR |
IL-37 was significantly downregulated in the skin barrier of children with AD.
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| Japan 2022; Tsuji et al. [14] |
normal human epidermal keratinocytes |
The upregulation of IL-37 in normal human epidermal keratinocytes by Tapinarof and Galactomyces ferment filtrate was blocked by the suppression of aryl hydrocarbon receptor (AHR). IL-37 increased the expression of IL-33. Tapinarof and Galactomyces ferment filtrate inhibited IL-37 expression.
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| United States of America 2021; Zhou et al. [15] |
skin and blood samples from moderate-to-severe AD treated with topical corticosteroid and those with no topical medications applied to skin for a period of at least 1 week |
A substantial decrease in IL1F7 transcripts (encoding IL-37) was observed in AD patient samples, which correlated with decreased transcript levels for important skin barrier function genes. The addition of Th2 cytokines to the skin model was sufficient to reduce epidermal IL-37 levels and develop critical characteristics of AD skin.
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| Norway 2020; Lossius et al. [16] |
16 adult patients (5 males, 11 females; mean age 32, range 20–73); patients received standard full-body nb-UVB therapy 3×/week for 6–8 weeks with a starting dose of 0.1–0.2 J/cm2 and progressive dose increase; analysis of different questionnaire of AD severity |
After treatment with nb-UVB, the pro-inflammatory IL-36 decreased, while the anti-inflammatory IL-37 increased.
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| China 2021; Hou et al. [17] |
blood samples from 20 healthy control subjects (aged 14–57 years) without history of skin, allergic, or inflammatory disease, and 34 subjects (aged 11–49 years) with moderate-to-severe AD; human HaCaT keratinocytes and 3D keratinocytes |
Levels of IL-37 and its receptor IL18R were significantly reduced in AD patients. A negative correlation was observed between IL-37 and involucrin, and IL-37 was shown to suppress involucrin expression in in vitro epidermal cell models.
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| Denmark 2022; Hu et al. [18] |
30 patients with AD and 30 healthy controls; 393 skin samples from multiple anatomical regions and time points; 1.5 mm minipunch biopsies for obtaining multiple full-thickness skin samples from the same subject over time |
The expression of IL-37 decreased in descending order from healthy controls to non-lesional to lesional tissues.
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