Reviews of Interleukin-37: Functions, Receptors, and Roles in Diseases

Jia, Honglei; Liu, Jing; Han, Bo

doi:10.1155/2018/3058640

Cited by 80 publications

(81 citation statements)

References 88 publications

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“…39 Many studies have shown that IL-37 plays an important regulatory role in various inflammatory diseases (eg, asthma), autoimmune diseases (eg, rheumatoid arthritis), and tumors. 40 A number of studies show that it is downregulated in patients with severe keloids: the recent cross-sectional study by Khattab et al showed that the IL-37 serum levels of keloid patients correlated inversely with keloid severity, as determined by the Japan Scar Workshop Scar Scale (JSW) (r = −0.737, P = .0001). In contrast, the serum IL-37 levels did not correlate with patient gender, age, keloid duration, or family history.…”

Section: Il-37mentioning

confidence: 99%

Systemic factors that shape cutaneous pathological scarring

Huang

Ogawa

2020

FASEB j.

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Cutaneous pathological scars are fibrotic lesions that grow continuously, invade the adjacent skin, and are erythematous, itchy, and painful. Their etiology remains unclear but may involve genetic, local mechanical, and systemic factors. Here, we will summarize the main systemic factors that shape cutaneous pathological scarring, especially keloid formation and aggravation. They include circulating cytokines, chemokines, growth factors, particular cell types, sex hormones, the systemic renin‐angiotensin system, and vitamin D, all of which directly shape the angiogenesis, inflammation, fibrosis, and remodeling in pathological scars. There are also several environmental factors that more indirectly influence pathological scar formation or progression, namely diet, smoking, psychological stress, and exercise. Notably, much of the evidence on these systemic factors focus on their effects on one pathological scar characteristic, namely their fibrosis. However, systemic factors probably also shape other pathological scar characteristics. We describe two new avenues of keloid research that may greatly improve our understanding of pathological scarring and the systemic factors that affect it. One is the multiple similarities between keloids and tumors; the other is the different stem‐cell populations in keloids. We expect this research will greatly aid the development of diagnostic biomarkers for cutaneous pathological scars and drugs/techniques/regimens that prevent, improve, or cure these scars.

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Section: Il-37mentioning

confidence: 99%

Systemic factors that shape cutaneous pathological scarring

Huang

Ogawa

2020

FASEB j.

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“…IL‐37b is the longest transcript variant. IL‐37 expression is detected in numerous tissues and immune cells such as thymus, bone marrow, lymph nodes, NK cells, monocytes, B cells . In recent years, IL‐37 has been shown to have significant effects on inhibiting inflammation in autoimmune diseases.…”

Section: Introductionmentioning

confidence: 99%

Elevated expression of interleukin‐37 in patients with rheumatoid arthritis

et al. 2019

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Aim This study aims to discuss plasma and messenger RNA (mRNA) levels of interleukin (IL)‐37 in rheumatoid arthritis (RA) patients and evaluate the potential of plasma IL‐37 as a biomarker for RA. Method Plasma IL‐37 levels and IL‐37 mRNA relative concentrations were measured by enzyme‐linked immunosorbent assay (ELISA) and quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR). We discussed the association of IL‐37 levels and clinical, laboratory parameters in RA patients in a training cohort. Plasma IL‐37 levels were tested for discriminatory capacity by receiver operating characteristic (ROC) curve analysis. We then validated plasma IL‐37 expression in a cohort of 598 patients (230 RA, 107 systemic lupus erythematosus [SLE], 100 osteoarthritis [OA], 62 gout, 51 primary Sjögren's syndrome [pSS], 48 ankylosing spondylitis [AS]). Results Both plasma levels of IL‐37 and mRNA levels of IL‐37 were elevated in RA patients compared to those in healthy controls in the training cohort, and there was a good diagnostic ability to predict RA (area under the curve [AUC] = 0.97). Plasma IL‐37 levels were significantly related to Disease Activity Score of 28 joints ‐ erythrocyte sedimentation rate (DAS28‐ESR) (rs = 0.459, P < 0.001). The levels of IL‐37 mRNA were related to plasma IL‐37 levels (rs = 0.642, P < 0.001), DAS28‐ESR (r = 0.641, P < 0.001) and C‐reactive protein (rs = 0.603, P < 0.001). In the validation cohort, when plasma IL‐37 in RA patients compared with that in SLE, OA, gout, pSS and AS patients, the AUC was 0.86, 0.87, 0.91, 0.87, 0.92, respectively. Conclusion IL‐37 expression was increased in RA patients, and correlated with disease activity. IL‐37 may be a biomarker for the diagnosis of RA.

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“…Although no specific receptor for IL-37 has been identified, a number of studies showed that extracellular IL-37 binds to the alpha chain of the IL-18Rα (36,37), but with much lower binding affinity than that of IL-18 (38). Moreover, IL-37 binds to an IL-18 binding protein (IL-18BP) (39), and to the decoy receptor 8 (IL-R8) (40) via which IL-37 inhibits innate inflammation (35,41,42) in vitro and in vivo (42).…”

mentioning

confidence: 99%

IL-37 is increased in brains of children with autism spectrum disorder and inhibits human microglia stimulated by neurotensin

Tsilioni

Patel

Pantazopoulos

et al. 2019

Proc. Natl. Acad. Sci. U.S.A.

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Autism spectrum disorder (ASD) does not have a distinct pathogenesis or effective treatment. Increasing evidence supports the presence of immune dysfunction and inflammation in the brains of children with ASD. In this report, we present data that gene expression of the antiinflammatory cytokine IL-37, as well as of the proinflammatory cytokines IL-18 and TNF, is increased in the amygdala and dorsolateral prefrontal cortex of children with ASD as compared to non-ASD controls. Gene expression of IL-18R, which is a receptor for both IL-18 and IL-37, is also increased in the same brain areas of children with ASD. Interestingly, gene expression of the NTR3/sortilin receptor is reduced in the amygdala and dorsolateral prefrontal cortex. Pretreatment of cultured human microglia from normal adult brains with human recombinant IL-37 (1 to 100 ng/mL) inhibits neurotensin (NT)-stimulated secretion and gene expression of IL-1β and CXCL8. Another key finding is that NT, as well as the proinflammatory cytokines IL-1β and TNF increase IL-37 gene expression in cultured human microglia. The data presented here highlight the connection between inflammation and ASD, supporting the development of IL-37 as a potential therapeutic agent of ASD.

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Reviews of Interleukin-37: Functions, Receptors, and Roles in Diseases

Cited by 80 publications

References 88 publications

Systemic factors that shape cutaneous pathological scarring

Systemic factors that shape cutaneous pathological scarring

Elevated expression of interleukin‐37 in patients with rheumatoid arthritis

IL-37 is increased in brains of children with autism spectrum disorder and inhibits human microglia stimulated by neurotensin

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