Version 5.4
| Mus musculus Gene: Il17a | |||||||||||||||||||||||
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| Summary | |||||||||||||||||||||||
| InnateDB Gene | IDBG-136575.6 | ||||||||||||||||||||||
| Last Modified | 2014-10-13 [Report errors or provide feedback] | ||||||||||||||||||||||
| Gene Symbol | Il17a | ||||||||||||||||||||||
| Gene Name | interleukin 17A | ||||||||||||||||||||||
| Synonyms | Ctla-8; Ctla8; IL-17; IL-17A; Il17 | ||||||||||||||||||||||
| Species | Mus musculus | ||||||||||||||||||||||
| Ensembl Gene | ENSMUSG00000025929 | ||||||||||||||||||||||
| Encoded Proteins |
interleukin 17A
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| Protein Structure | |||||||||||||||||||||||
| Useful resources | Stemformatics EHFPI ImmGen | ||||||||||||||||||||||
| InnateDB Annotation | |||||||||||||||||||||||
| Summary |
Il17a signalling enhances the mRNA stability of chemokine Cxcl1 through Traf3ip2, Traf2-Traf5 and the RNA-binding protein Srsf1.
Il17a is significantly upregulated in both S. pyogenes inoculated and mock inoculated mice, indicating that the cytokine production can be triggered by inoculation trauma alone.
IL17A inhibits the release of IL23 during pulmonary inflammation and serves as part of negative feedback loop to control antibacterial immunity.
Il17a is an intrinsic regulator in coordinating neutrophil and macrophage antimicrobial activity to provide protection against acute pneumonic plague.
In mouse model of leukocyte adhesion deficiency type I disease, defective neutrophil recruitment is associated with dysregulated local overproduction of IL17, which drives inflammatory periodontal bone loss.
Defb1 is important for the control of early mucosal Candida infection and plays a critical role in the induction of innate inflammatory mediators including, Il1b, Il6, Cxcl1, Il17a, and Il17f.
Il17a is rapidly produced during lung injury and significantly contributes to early immunopathogenesis, a process that is orchestrated largely by a distinct population of pulmonary type 3 innate lymphoid cells.
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| InnateDB Annotation from Orthologs | |||||||||||||||||||||||
| Summary |
[Homo sapiens] IL17A is a cytokine produced by T helper 17 (Th17) cells that plays important roles in the development of inflammatory diseases.
[Homo sapiens] IL17A is an innate-adaptive immunomodulatory cytokine that is produced by gammadelta cells and is a key mediator for the innate immune response to urinary tract infections (UTIs) caused by uropathogenic Escherichia coli.
[Homo sapiens] IL17A is a Th17-related cytokine, traditionally thought of as an adaptive responder, has been shown to have various innate sources and functions as a rapidly produced pro-inflammatory mediator. Innate IL17A-producing cells also employ many of the cytokine and transcriptional regulators utilized by Th17 cells.
[Homo sapiens] IL17A signalling enhances the mRNA stability of chemokine CXCL1 through TRAF3IP2, TRAF2-TRAF5 and the RNA-binding protein SRSF1.
[Homo sapiens] IL17A is significantly upregulated in both S. pyogenes inoculated and mock inoculated mice, indicating that the cytokine production can be triggered by inoculation trauma alone. (Demonstrated in mice)
[Homo sapiens] Local production of IL17A in the airways drives early neutrophil infiltration into respiratory syncytial virus infected infant lungs.
[Homo sapiens] IFNG interferes with the IL-1/NFKBIZ axis in β-glucan-activated dendritic cells and promotes T cell-mediated immune responses with increased release of IFNG and IL22, and diminished production of IL17A.
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| Entrez Gene | |||||||||||||||||||||||
| Summary |
This gene does not have any Entrez summary - the following is the summary from its human ortholog ENSG00000112115:
The protein encoded by this gene is a proinflammatory cytokine produced by activated T cells. This cytokine regulates the activities of NF-kappaB and mitogen-activated protein kinases. This cytokine can stimulate the expression of IL6 and cyclooxygenase-2 (PTGS2/COX-2), as well as enhance the production of nitric oxide (NO). High levels of this cytokine are associated with several chronic inflammatory diseases including rheumatoid arthritis, psoriasis and multiple sclerosis. [provided by RefSeq, Jul 2008] |
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| Gene Information | |||||||||||||||||||||||
| Type | Protein coding | ||||||||||||||||||||||
| Genomic Location | Chromosome 1:20730905-20734496 | ||||||||||||||||||||||
| Strand | Forward strand | ||||||||||||||||||||||
| Band | A4 | ||||||||||||||||||||||
| Transcripts |
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| Interactions | |||||||||||||||||||||||
| Number of Interactions |
This gene and/or its encoded proteins are associated with 24 experimentally validated interaction(s) in this database.
They are also associated with 7 interaction(s) predicted by orthology.
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| Gene Ontology | |||||||||||||||||||||||
Molecular Function |
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| Biological Process |
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| Cellular Component |
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| Orthologs | |||||||||||||||||||||||
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Species
Homo sapiens
Bos taurus
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Gene ID
Gene Order
Not yet available
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| Pathways | |||||||||||||||||||||||
| NETPATH | |||||||||||||||||||||||
| REACTOME | |||||||||||||||||||||||
| KEGG |
Cytokine-cytokine receptor interaction pathway
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| INOH |
JAK STAT pathway and regulation pathway
GPCR signaling pathway
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| PID NCI | |||||||||||||||||||||||
| Pathway Predictions based on Human Orthology Data | |||||||||||||||||||||||
| NETPATH | |||||||||||||||||||||||
| REACTOME | |||||||||||||||||||||||
| KEGG |
Cytokine-cytokine receptor interaction pathway
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| INOH |
JAK STAT pathway and regulation pathway
GPCR signaling pathway
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| PID NCI |
IL27-mediated signaling events
IL23-mediated signaling events
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| Cross-References | |||||||||||||||||||||||
| SwissProt | |||||||||||||||||||||||
| TrEMBL | |||||||||||||||||||||||
| UniProt Splice Variant | |||||||||||||||||||||||
| Entrez Gene | |||||||||||||||||||||||
| UniGene | Mm.5419 | ||||||||||||||||||||||
| RefSeq | NM_010552 | ||||||||||||||||||||||
| OMIM | |||||||||||||||||||||||
| CCDS | CCDS14842 | ||||||||||||||||||||||
| HPRD | |||||||||||||||||||||||
| IMGT | |||||||||||||||||||||||
| MGI ID | |||||||||||||||||||||||
| MGI Symbol | |||||||||||||||||||||||
| EMBL | |||||||||||||||||||||||
| GenPept | |||||||||||||||||||||||
| RNA Seq Atlas | |||||||||||||||||||||||