Expression of interleukin (IL)-19 and IL-24 in inflammatory bowel disease patients: a cross-sectional study

Fonseca‐Camarillo, Gabriela; Furuzawa‐Carballeda, Janette; Granados, Jesús Benítez; Yamamoto-Furusho, Jesús K.

doi:10.1111/cei.12285

Cited by 59 publications

(59 citation statements)

References 29 publications

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“…Very interestingly, two recent clinical trials have demonstrated that anti-IL-20 monoclonal antibody is effective in the treatment of RA and psoriasis [59, 60]. Furthermore, levels of IL-19, IL-20, IL-24 and IL-26 are also elevated in serum of patients with inflammatory bowel disease [61–64], which is associated with the intergenic 6q23 variants tagged by rs6920220 [25]. The evidence that SNPs associated with different autoimmune diseases interact with each other and the same genes supports a concept that regional genetic variation, regulating similar target genes, but with mechanistic and cellular differences, are risk factors for different diseases.…”

Section: Discussionmentioning

confidence: 99%

Capture Hi-C identifies a novel causal gene, IL20RA, in the pan-autoimmune genetic susceptibility region 6q23

et al. 2016

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BackgroundThe identification of causal genes from genome-wide association studies (GWAS) is the next important step for the translation of genetic findings into biologically meaningful mechanisms of disease and potential therapeutic targets. Using novel chromatin interaction detection techniques and allele specific assays in T and B cell lines, we provide compelling evidence that redefines causal genes at the 6q23 locus, one of the most important loci that confers autoimmunity risk.ResultsAlthough the function of disease-associated non-coding single nucleotide polymorphisms (SNPs) at 6q23 is unknown, the association is generally assigned to TNFAIP3, the closest gene. However, the DNA fragment containing the associated SNPs interacts through chromatin looping not only with TNFAIP3, but also with IL20RA, located 680 kb upstream. The risk allele of the most likely causal SNP, rs6927172, is correlated with both a higher frequency of interactions and increased expression of IL20RA, along with a stronger binding of both the NFκB transcription factor and chromatin marks characteristic of active enhancers in T-cells.ConclusionsOur results highlight the importance of gene assignment for translating GWAS findings into biologically meaningful mechanisms of disease and potential therapeutic targets; indeed, monoclonal antibody therapy targeting IL-20 is effective in the treatment of rheumatoid arthritis and psoriasis, both with strong GWAS associations to this region.Electronic supplementary materialThe online version of this article (doi:10.1186/s13059-016-1078-x) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Capture Hi-C identifies a novel causal gene, IL20RA, in the pan-autoimmune genetic susceptibility region 6q23

et al. 2016

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“…Serum levels of IL-19, IL-20, IL-24 and IL-26 are elevated in patients with active IBD versus those with inactive IBD or healthy controls 92,[113][114][115] . However, unlike IL-22RA1, IL-20RA and IL-20RB are not highly expressed in the intestine 5,20 .…”

Section: Il-20 Subfamily Cytokines In Inflammatory Diseasementioning

confidence: 95%

The IL-20 subfamily of cytokines — from host defence to tissue homeostasis

Rutz¹,

Wang²,

Ouyang³

2014

Nat Rev Immunol

290

296

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The interleukin-20 (IL-20) subfamily of cytokines comprises IL-19, IL-20, IL-22, IL-24 and IL-26. These cytokines are all members of the larger IL-10 family, but have been grouped together to form the IL-20 subfamily based on their usage of common receptor subunits and similarities in their target-cell profiles and biological functions. Members of the IL-20 subfamily facilitate the communication between leukocytes and epithelial cells, thereby enhancing innate defence mechanisms and tissue repair processes at epithelial surfaces. In this Review, we describe the cellular sources and targets of the IL-20 subfamily cytokines, and we detail how their expression is regulated. Much of our understanding of the unique biology of this group of cytokines is still based on IL-22, which is the most studied member of the IL-20 subfamily. Nevertheless, we attempt a broader discussion of the emerging functions of IL-20 subfamily cytokines in host defence, inflammatory diseases, cancer and metabolism.

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“…Nonetheless, several immune-regulatory mediators such as some members of IL-10 family and IDO (Indoleamine 2,3-dioxygenase) are up-regulated in the intestinal mucosa of patients with IBD [3][4][5].…”

Section: Introductionmentioning

confidence: 99%

Interleukin 35 (IL-35) and IL-37: Intestinal and peripheral expression by T and B regulatory cells in patients with Inflammatory Bowel Disease

2015

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Expression of interleukin (IL)-19 and IL-24 in inflammatory bowel disease patients: a cross-sectional study

Cited by 59 publications

References 29 publications

Capture Hi-C identifies a novel causal gene, IL20RA, in the pan-autoimmune genetic susceptibility region 6q23

Capture Hi-C identifies a novel causal gene, IL20RA, in the pan-autoimmune genetic susceptibility region 6q23

The IL-20 subfamily of cytokines — from host defence to tissue homeostasis

Interleukin 35 (IL-35) and IL-37: Intestinal and peripheral expression by T and B regulatory cells in patients with Inflammatory Bowel Disease

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