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Validated All-in-One™ qPCR Primer for IL17A(NM_002190.2) Search again
Product ID:
HQP009717
(click here to view gene annotation page)
Powered by BiozSpecies:
Human
Symbol:
Alias:
CTLA-8, CTLA8, IL-17, IL-17A, IL17, ILA17
Gene Description:
interleukin 17A
Target Gene Accession:
NM_002190.2(click here to view gene page)
Estimated Delivery:
Approximately 1-3 weeks, but may vary. Please email sales@genecopoeia.com or call 301-762-0888 to confirm ETA.
Important Note:
By default, qPCR primer pairs are designed to measure the expression level of the splice variant (accession number) you selected for this gene WITHOUT consideration of other possible variants of this gene. If this gene has multiple variants, and you would like to measure the expression levels of one particular variant, multiple variants, or all variants, please contact us for a custom service project at inquiry@genecopoeia.com.
Validated result:
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| A | B |
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Each All-in-One™ qPCR Primer is experimentally validated to yield a single dissociation curve peak and to generate a single amplification of the correct size for the targeted gene. A cDNA Pool, containing reverse transcript products of 8 different human tissue total RNA(Liver, Testis,Muscle,Thyroid,Brain,Spleen,Stomach,Small Intestine)),was used as the qPCR validation template. qPCR was performed using 0.2 µM primer with 2XAll-in-One™ qPCR Mix (Catalog#: QP001,QP002,QP004,QP005). Reactions were incubated for 10min. at 95°C, followed by 40 cycles of 95°C for 10 sec.; 60°C, 20 sec. and 72°C, 15sec. using Bio-Rad iQ5™ Instrument. At the end of the last cycle, temperature was increased from 72 to 95°C to produce a melting curve. Panel A: Validated Result for Amplification Curve; Panel B: Validated Result for Melting Curve. |
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Summary
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].
Gene References into function
- IL-17 selectively down-regulates TNF-alpha-induced RANTES gene expression in human colonic subepithelial myofibroblasts.
- activation of the ERK pathway is involved in the induction of IL-6 mRNA stabilization by IL-17 plus TNF-alpha.
- IL-17 induces a signaling cascade involving src-MAPK activation in human cells
- IL-17 plays an important role in the induction and perpetuation of the immunopathologic processes in herpetic stromal keratitis by modulating the secretion of proinflammatory and neutrophil chemotactic factors by corneal resident fibroblasts.
- Low levels of IL-17 in combination with IL-1 beta can act on myoblasts and muscle tissue leading to the expression or production of factors involved in muscle inflammation.
- IL-17 may play important role in homeostasis via IL-6 upregulation and in regulating inflammation of prostate
- could have a significant role in the progression of gingivitis to periodontitis
- transcriptional activation of the IL17 gene by Tax protein of HTLV-1 virus.
- upregulation of interleukin 17 is associated with cutaneous T-cell lymphomas
- In Helicobacter pylori-colonized gastric epithelial cells, IL-17-induced IL-8 synthesis is associated with and depends at least in part on the activation of ERK 1/2 MAP kinase.
- IL-17 and IL-17F play a differential regulatory role in GM-CSF production by LMVECs stimulated with IL-1beta and/or TNF-alpha, which is sensitive to Th1 and Th2 cytokine modulation
- NFAT is the crucial sensor of TCR signaling in the IL-17 promoter.
- Review. IL-17 has proinflammatory properties, particularly the induction of other inflammatory effectors. It synergizes with other cytokines, placing it in the center of the inflammatory network. It is implicated in bone diseases & rheumatoid arthritis.
- Review. IL-17 is significant when T cells are a major element of the arthritis process. IL-17 can induce joint destruction in an IL-1-independent manner & can bypass TNF-dependent arthritis.
- has a potential role in the aetiopathogenesis of periodontal disease
- total amount in gingival crevicular fluid samples and in the culture supernatants of gingival cells is significantly increased in periodontal disease
- IL-17 particularly affects post-transcriptional regulation of IL-8 and IL-6 expression leading to enhanced IL-8 and IL-6 responses to secondary stimuli, and is only a weak proinflammatory stimulus by itself
- The fact that the increased IL-17A mRNA is associated with an increased number of MMP-9-expressing neutrophils is compatible with IL-17A increasing the local proteolytic burden through its neutrophil-accumulating effect.
- cell membrane IL-17R is required for signaling by both IL-17A and IL-17F
- Data suggest that IL-17 may play an important role in the inflammatory response to Helicobacter pylori colonization of gastric mucosa.
- In this JEG-3 cell model of human trophoblast, IL-17 may have a regulatory role in trophoblast invasion.
- Inhibitors of MEK abrogated the mitogenic effect of IL-17A, whereas an inhibitor of p38 or JNK displayed no significant inhibitory effect.IL-17A stimulates the growth of airway epithelial cells through the ERK MAP kinase pathway.
- The data suggest that Th17 cell infiltration in asthmatic airways links T cell activity with neutrophilic inflammation in asthma.
- plays a role as a key regulatory cytokine [in periodontitis]
- human T helper cells-17 cells have distinct migratory capacity and antigenic specificities
- IL-17A can modify epithelial responses to rhinovirus in a manner that would be expected to favor the recruitment of neutrophils, immature dendritic cells, and memory T cells to the airways
- IL-17 is associated with the early post-lung transplantation time period and airway CD8+ cells.
- analysis of functional features of human Th17 cells
- S100A8 is regulated by IL-17, dexamethasone, IL-4 and IL-13 in HaCat cells (human keratinocyte cell line)
- IL-17A activity is an important element of pulmonary host defence, but the prolonged action of this cytokine directed on the proliferation, maturing and chemotaxis of neutrophils to the pulmonary tract may contribute to chronic tissue destruction.
- Our results provided the first evidence that -197A (IL-17A) and 7488T (IL-17F) alleles may influence the susceptibility to and pathophysiological features of ulcerative colitis independently.
- These results provide the first evidence that the IL-17F and MIF gene polymorphisms are significantly associated with the development of functional dyspepsia.
- Data suggest that IL-17-dependent cellular immunity to collagen type V predisposes to obliterative bronchiolitis in human lung transplants.
- two independent and indispensable signaling pathways-1) JAK1-associated PI3K signaling and 2) Act1/TRAF6/TAK1-mediated NF-kappaB activation-are stimulated by IL-17A to regulate gene induction in human airway epithelial cells.
- Il-17 producing T cells are important in mucosal host defense, in the setting of retained antigenic stimulation, such as in asthma, chronic infection, and cystic fibrosis, or in the setting of autoimmunity, these cells can mediate immunopathology [review
- IL-17A enhances the expression of cyclooxygensase-2 and IL-8 and the proliferation of endometriotic stromal cells. IL-17A may play a role in the development of endometriosis.
- IL-17 gene expression in synovial tissues of Rheumatoid arthritis (RA) was similar to that in Osteoarthritis; expression level in peripheral blood monouclear cells of RA was significantly higher than controls
- All IL-17-producing CD4+ T cells expressed CCR6, a receptor found on approximately 50% of CD4+ memory peripheral blood leukocytes.
- there is an enrichment of both IL-17+CD4+ and CD8+ T cells in active multiple sclerosis lesions
- analysis of an IL-17A-dependent pathway of dendritic cell fusion in langerhans cell histiocytosis
- Interleukin 17 levels are increased in juvenile idiopathic arthritis synovial fluid and induce synovial fibroblasts to produce proinflammatory cytokines and matrix metalloproteinases
- Immunohistochemical stainings of submandibular glands from C57BL/6.NOD-Aec1Aec2 mice and of salivary gland biopsy specimens from Sjogren's syndrome patients revealed IL-17 and IL-23 staining within lymphocytic foci and epithelial tissues.
- Proinflammatory cells in juvenile idiopathic arthritis contribute to joint pathology, as indicated by relationships with clinical phenotypes, and that the balance between IL-17+ T cells and Treg cells may be critical to outcome.
- Il-17 may be involved in autoimmune responses in systemic sclerosis
- data suggest that the inability to produce T(H)17 cells is a mechanism underlying the susceptibility to the recurrent infections commonly seen in autosomal dominant hyper-IgE syndrome
- the NF-kappaB binding cofactor, IkappaB-zeta, was up-regulated by IL-17A, and the knockdown of IkappaB-zeta significantly diminished the IL-17A-induced hBD-2 expression.
- The activated IL-23/IL-17 axis is important for the inflammatory immunity in systemic lupus erythematosus.
- High levels of IL-1beta, IL-10, IL-17 and TNF-alpha (in the serum and synovial fluid) were observed in arthritis compared to the healthy controls.
- Review highlights the developmental pathways shared by new lineage, IL-17-producing CD4+ T helper (Th17) cells and regulatory T cell subsets during the pathogenesis or control of inflammation.
- The number of Th17 cells is increased in the peripheral blood and acute lesional skin of atopic dermatitis. Th17 cells may exaggerate atopic eczema.
- Foxp3 inhibits RORgammat-mediated IL-17A mRNA transcription through direct interaction with RORgammat
- some memory Th-17 cells might play an important role in the defense against the infections of fungi such as C. albicans
- IL-17 and TLR2 ligands stimulate the production of IL-16 by rheumatoid arthritis fibroblast-like synoviocytes
- tumor-induced TGF-beta may actively subvert the CD8+ arm of the immune system into directly promoting tumor growth by an IL-17-dependent mechanism
- Results show that the OX40-OX40L interaction suppresses IL-17 production by PHA-stimulated human PBMC and purified CD4 and CD8 cells.
- IL-17 family members are varyingly expressed in rheumatoid nodules. The paucity of IL-17A in nodules suggests an important difference from that observed in the synovium
- Levels of IL-23, IL-17, and IFN-gamma are elevated in Behcet disease(BD) with active uveitis. IL-23/IL-17 pathway together with IFN-gamma is associated with active intraocular inflammation in BD patients.
- multiple myeloma patients without osteonecrosis of the jaw and control subjects presented similar values of IL-17 serum levels
- The expression level of IL-17A was significant difference in expression between gingivitis and periodontitis .
- a failure of CD4+ T cells harboring heterozygous STAT3 mutations to generate interleukin 17-secreting cells due to a failure to express sufficient levels of the Th17-specific transcriptional regulator retinoid-related orphan receptor t.
- IL-12Rbeta1- and STAT-3--dependent signals play a key role in the differentiation and/or expansion of human IL-17-producing T cell populations in vivo.
- No significant differences of IL-17 concentration were observed between patients with active immune thrombocytopenic purpura and the control group
- this study provides the first evidence that serum IL-17 levels might be increased in patients monosensitized to birch with the most severe allergic rhinitis. Thus increased IL-17 serum levels can be considered a marker of severe allergy.
- Peripheral blood mononuclear cells from immunocompetent Candida-infected patients secreted more IL-17 and IL-22 than those of both chronic mucocutaneous candidiasis patients and healthy, non-infected controls.
- regulatory T cells (CD4(pos)CD25(high)Foxp3(pos)CD127(neg)CD27(pos)) can differentiate into IL-17-producing cells, when stimulated by allogeneic antigen-presenting cells, especially monocytes, in the presence of rhIL-2/rhIL-15.
- all IL-17-producing cells originate from CD161(+) naive CD4(+) T cells of umbilical cord blood, as well as of the postnatal thymus
- These data demonstrate the capacity of dendritic cells (DCs) to induce expansion of polyfunctional IL17-producing T cells in humans, and suggest a role for DCs in the enrichment of Th17-1 cells in the tumor bed.
- Human IL-17F/IL-17A heterodimer can bind and signal through the same receptor complex as homodimeric cytokines IL-17F and IL-17A.
- Th17-secreting cells detected in the salivary glands of Sjogren's syndrome (SS) patients are associated with the pathogenesis of SS in the salivary glands.
- The role of the IL23/IL17 axis in bronchiolitis obliterans syndrome after lung transplantation is reported.
- Our data suggest that IL17 might play a crucial role mainly in the early phase of MS, while IFNgamma seems to be involved both in the early phase and in the following relapses of the disease.
- Prevalence, phenotype and distribution of IL-17-expressing T cells is demonstrated in the skin of psoriasis patients, revealing that psoriatic skin contains abundant IL-17-positive T cells including T helper (Th)17 cells and CD8+ IL-17-expressing T cells
- IL-17A increased pneumococcal killing by human neutrophils both in the absence and in the presence of antibodies and complement
- regulation of human CD4+ IL-17-producing T cells in ovarian cancer.
- IFNalpha down-regulates IL-17 expression and Th17 differentiation in vitro and in vivo.
- In the presence of antigen-presenting cells, T helper cell interleukin (IL)-17 production is enhanced by IL-1 and IL-23.
- IL-17 expression is increased in human asthmatic alveolar macrophages, but not IL-17-positive interstitial macrophages, after allergen challenge.
- In cultured tumor cells, IL-17 strongly represses tumor necrosis factor-alpha-stimulated expression of chemokines CXCL10, CXCL11 and CCL5, but synergizes with TNF-alpha for induction of CXCL8, CXCL1 and CCL20 mRNAs.
- RORgamma controls IL-17A and IL-17F production, and these cytokines have a redundant but highly pathogenic role in gut inflammation.
- IL-17A enhances cathelicidin expression in keratinocytes through activation of Act1, an adaptor protein involved in IL-17A signaling, and a Map kinase-ERK kinase-dependent mechanism.
- IL-17 production is increased in systemic lupus erythematosus patients due to the expansion of the proinflammatory double negative T cell subset and to excessive IL-17 production of CD4-positive T cells.
- The ineffective IL-17-dependent upregulation of HBD-2 in patients with AE is due to a partial inhibition by the type 2 microenvironment, which could partially explain why patients with AE do not clear S aureus.
- Data suggest that graft-derived IL-1 can promote T cell intimal recruitment and IL-17 production during human artery allograft rejection, and suggest that targeting IL-1 in the perioperative transplant period may modulate host alloreactivity.
- Skin-migratory dendritic cells stimulate allogeneic naive CD4+ T cells that differentiate simultaneously into two distinct effector T helper (Th)17 and Th1 populations capable of homing to the skin, where they induce severe cutaneous damage.
- Il-17 production occurs in intestinal biopsies of Celiac disease patients in response to gliadin.
- In alcoholic hepatitis, liver infiltration with IL-17-secreting cell infiltrates is a key feature that might contribute to liver neutrophil recruitment.