IL23A, interleukin 23 subunit alpha, 51561

N. diseases: 427; N. variants: 2
Source: ALL
Disease Score gda Association Type Type Original DB Sentence supporting the association PMID PMID Year
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE IL-6, IL-12, and IL-23 STAT-Pathway Genetic Risk and Responsiveness of Lymphocytes in Patients with Multiple Sclerosis. 30917537 2019
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE Cytokines of the Interleukin (IL)-12 family, consisting of IL-12, IL-23, IL-27 and IL-35, are important regulators in (chronic) inflammatory disorders such as rheumatoid arthritis and multiple sclerosis, but also in cardiovascular diseases. 29074035 2019
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 AlteredExpression disease BEFREE The results showed that IFN-β can reduce the proportion of Th17 cells, the levels of IL-17 and IL-23 in serum of MS. 31517556 2019
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE Interleukin 23 (IL-23) is a key mediator in neuroinflammation in numerous autoimmune diseases including multiple sclerosis (MS). 31154574 2019
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE Nevertheless, biological drugs that target the IL-23-IL-17 pathway are highly effective in treating human psoriasis and are showing promise in the treatment of relapsing remitting MS and other T-cell mediated autoimmune diseases. 29395738 2018
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE IL-12/IL-23 pathway plays a pivotal role in etiopathogenesis of multiple sclerosis (MS), suggested by studies both in patients and animal models. 28276258 2017
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE Our results suggest that the use of vectors carrying sIL-23R to block the IL-23/IL-23R interaction may be a new therapeutic strategy for the treatment of multiple sclerosis. 28593439 2017
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 AlteredExpression disease BEFREE Under random effect model of meta-analysis, the data showed that the proportion of Th17 cells in PB and levels of serum IL-17 and IL-23 increased among MS patients compared to control subjects. 29141810 2017
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 GeneticVariation disease BEFREE Three variants rs2066808, rs2371494, rs11575248 in <i>IL-23A</i> gene and one variant rs1884444 in <i>IL-23R</i> gene were demonstrated to be associated with the risk of MS or other IDD diseases, and the expression level of serum IL-23A in the MS patients was also altered. 27893410 2016
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE Finally, transcriptional over-expression of MR1 - which presents cognate antigens to MAIT cells - and of the activating cytokines IL-18 and IL-23 was evidenced in MS lesions, suggesting that the CNS microenvironment is suited to activate the few infiltrating MAIT cells. 27050759 2016
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE The IL-7/IL-7R signaling axis participates in cell survival, and perturbation of this pathway has been associated with enhanced susceptibility to MS. A link between IL-23-driven pathogenic T cells and IL-7/IL-7R signaling has previously been proposed, but has not been formally addressed. 26223651 2015
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 GeneticVariation disease BEFREE Association of IL-23 and its receptor gene single-nucleotide polymorphisms with multiple sclerosis in Chinese southern population. 24547735 2014
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE Pathogenic IL-23-dependent TH17 cells have been shown to be critical for the development of experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, and genetic risk factors associated with multiple sclerosis are related to the IL-23-TH17 pathway. 23467095 2013
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 AlteredExpression disease BEFREE Increased IL-10 mRNA and IL-23 mRNA expression in multiple sclerosis: interferon-beta treatment increases IL-10 mRNA expression while reducing IL-23 mRNA expression. 18424480 2008
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 AlteredExpression disease BEFREE We concluded that the p38 MAP kinase and NF-kappaB signaling pathways play an important role in regulation of IL-23p19 expression on human microglia, and are thus potential therapeutic targets in the treatment of MS. 18054783 2008
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE Increased IL-23 secretion and altered chemokine production by dendritic cells upon CD46 activation in patients with multiple sclerosis. 18403025 2008
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 AlteredExpression disease BEFREE Taken together, these findings on the expression of IL-23p19 in multiple sclerosis lesions may lead to a better understanding of the events culminating in human multiple sclerosis. 17003070 2007
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease BEFREE An important role for the IL-12/IL-23 pathway in multiple sclerosis (MS) is supported by immunologic studies in patients and animal models. 18082575 2007
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 AlteredExpression disease BEFREE Thus, IL-23 expression in DCs may play an important role in the pathogenesis of human autoimmune diseases such as MS. We quantified the expression of IL-23 in monocyte-derived DCs in MS patients and healthy donors and found that DCs from MS patients secrete elevated amounts of IL-23 and express increased levels of IL-23p19 mRNA. 16751425 2006
CUI: C0026769
Disease: Multiple Sclerosis
Multiple Sclerosis
0.100 Biomarker disease LHGDN Our results demonstrate that an abnormal Th1 bias in DCs from MS patients related to IL-23 exists, and that antisense oligonucleotides specific to IL-23 can be used for immune modulation by targeting DC gene expression. 16751425 2006