Interleukin-17B Antibodies

Interleukin-17B (IL17B)

Stimulates the release of tumor necrosis factor alpha and IL-1-beta from the monocytic cell line THP-1. .

Gene Information

Human
Gene Name:	IL17B
Uniprot:	Q9UHF5
Entrez:	27190

Family

Belongs to:
IL-17 family

Alternative Names

Cytokine Zcyto7; cytokine-like protein ZCYTO7; IL17B; IL-17B; IL-17Binterleukin-17 beta; IL20; IL-20interleukin-17B; interleukin 17B; interleukin 20; Interleukin-20; MGC138900; MGC138901; neuronal interleukin-17 related factor; Neuronal interleukin-17-related factor; NIRF; ZCYTO7interleukin-20

Molecular Weight

Mass (kDA):
20.437 kDA

Genomic Context

Human
Location:	5q32
Sequence:	5; NC_000005.10 (149374267..149404202, complement)

Tissue Specificity

Expressed in adult pancreas, small intestine, stomach, spinal cord and testis. Less pronounced expression in prostate, colon mucosal lining, and ovary.

Subcellular Localizations

Secreted.

Diseases

• Leprosy
• Tissue Adhesions
• Erythema
• Inflammation
• Radiation Injuries, Experimental
• Hypoxia
• Collagen Arthritis
• Hyperkeratosis
• Leukemia, Myelocytic, Acute
• Neoplasm, Residual
• Malignant Neoplasms

• Myeloid Leukemia
• Asthma
• Celiac Disease
• Rheumatoid Arthritis
• Cell Invasion

Pathways

• Cell Proliferation
• Pathogenesis
• Methylation
• Notch Signaling Pathway
• Regeneration
• Drug Resistance

PTMs

• Methylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IL17B

Best Uses Of The IL17B Marker

The IL17B marker was identified as a biomarker for many diseases, including leukemia. This protein is made by the immune system and plays an essential role in cellular health. In this article, we will discuss the ways in which IL-17B enhances the anti-mycobacterial activity of IFN-g and TNF-a. This information is available to scientists all over the world.

IL-17 improves the antimycobacterial activity in IFN-g

Type III IFNs stimulate innate immune responses within mice. These cells are activated to secrete certain molecules which regulate inflammation. The authors identified IL-17 as a novel antimycobacterial agent in mice. This study suggests that IL-17 could improve antimycobacterial activity in IFN-g mice. Future studies will focus on IL-17's role in the pathogenesis mycobacterial infection.

It is not clear what role IL-17 plays in the pathogenesis and progression of TB. This cytokine is necessary for survival of IFN-g-producing sputum-producing cell lines. It also promotes expansion of Th27 cells by increasing the number of CD4+ T cells. This has been linked to a decrease incidence of pulmonary tuberculosis among Southern Brazilians.

Although many studies have suggested a Th2-mediated TB defense, others have come to the opposite conclusion. Mtb infection occurs without IL-10 and results in decreased bacterial loads within the lung. The inflammatory response is also accelerated. The anti-mycobacterial effects of IFN-g are associated with an increase number CD4+ T cells. Moreover, both IL-17 and IL-10 are involved in chemokine production and have antimycobacterial activity.

In addition to IL-17, TNF and Mtb-mediated macrophage activation are crucial in controlling mycobacterial growth. TNF and GM -CSF are critical in the innate immune response against Mtb infection. Inhibiting IL-17 might improve this process and protect lung cells from the pathogen. This research could help us understand the role of IL-17 in Mtb's pathogenesis.

In mice, IL-17 induces expansion of CD4+IFN-g+ T-cells, which is associated with protection from Mtb challenge. This increased IFN-g+CD4+ was associated with protection against Mtb in mice who were immunized by BCG-primed HSP90–E6 vaccine. However, IL-17 was not able to induce maturation in the phagosome. However, it did enhance Mtb/LAMP1 coordination in mice. The result was comparable with 100 ng/mL IFN–g.

Cxcl10 and IL-17A levels were elevated in vaccinated mice with IFNg. Similar results were achieved through neutralization of IL-17 signalsling capacity. This supports previous findings that IL-17 cytokine inhibits IFN-g's anti-mycobacterial activities. It also shows that IL-17 can be a powerful immune system factor.

IL-17 might be an important cellular signal in innate immune reactions. Inflammatory responses are triggered by inflammation. Th27 cell role is crucial in pathogenesis. It is responsible for autoimmune disorders and increases the activity other immune cells. TNFa and IL-2 are essential for immune defense. There are many theories about this effect. Further research is needed to determine if they are involved.

It appears that IL-17 also promotes the development of an effective anti-mycobacterial response in mice with mycobacterial infection. During Mtb infection, mice with IL-17 lack the cytokine IL-10 and exhibit enhanced protection against the disease. The increased protection from Mtb infection is associated with an accelerated Th2 response in the lung and spleen. However, it is unclear whether the increased CXCL10 production is directly related to IL-17.

TNFa is more anti-mycobacterial than IFN-g thanks to IFN-g

The cytokine TNF is essential for anti-mycobacterial immunity and plays a central role in mycobacteria. It increases the phagocytic power of macrophages, and it enhances killing intracellularly viable bacteria. It can be combined with interferon-g. If TNF is blocked mycobacterial growth occurs in granulomas and chronic latent diseases. Mice without TNF or the TNFRp55 gene die prematurely from tuberculosis, Listeria monocytogenes and other infections.

IFN-g pretreatment also increased anti-mycobacterial activities of CD8 T cell, which is important for immunotherapy of cancer and chronic viruses infections. These findings are important for designing anti-mycobacterial immunotherapy. It also supports the hypothesis that IFNg increases anti-mycobacterial action of TNFa.

Studies have shown IFNg-g to increase TNFa's antimycobacterial activity in mice. It facilitates the priming of naive and naive immune cells in vivo. These mice were also less likely to reject OVA skin grafts than controls. However, IFNg-/ mice failed to reject recent OVA skin grafts. These mice were not immune against OVA when grafted using the anti-IFNg antibody.

These preliminary findings are not conclusive. TNF ANTAGONISTS have to be tested against TB in more studies. These findings support TNF antagonists as a treatment option for latent TB. These drugs could potentially reduce TB cases, and even prevent TB death. TNF ANTAGONIST TREATINGS cannot be denied.

TNF-a's antimycobacterial activity may be enhanced by IFN-g, which inhibits autophagy. These results show that IFN-1g may increase TNF-a’s anti-mycobacterial activities. IFN-g also inhibits autophagy, which is a process in which cells recycle the damaged proteins. The inhibitory effects of TNF-a on autophagy are the key to preventing infection.

Research has shown that IFNg can inhibit macrophages from producing IL-12. These cytokines can be important for anti-tumour immune system. TNF-a, however, suppresses IFN g production through a mechanism that is still not fully understood. Although IFN-g inhibits IL-12 production, it promotes TNF-a and IL-1b production.

TNF-a and TNF-g have been positively affected by the anti-TNF monoclonal antibody, IFN-g. However, there is no evidence that IFNgg enhances TNF-a's anti-TB activities in humans. There is a high chance of side effects from the use of this drug in humans.

Infliximab first became available in 2000 for the treatment of psoriasis. The drug also had remarkable results in a patient who had Crohn's disease. Numerous other studies have confirmed that TNF antagonists are effective in treating psoriasis. It is currently being evaluated for other indications in inflammatory skin conditions.

TNF-a

Boster Bio is developing a soluble immunogen for use in a vaccine against pneumonic plague. The IL-17B marker is part of a gene coding for IL-23, which has numerous uses in the immune system. It is a variable protein that is produced in response inflammatory stimuli. The best method to measure IL-23 level is to use the bosterbio.il17b mark.

Researchers at the University of Chicago Medical Center, and the Massachusetts General Hospital identified three types of IL-17B marker. IL-17C, a protein expressed in synovial fluid as well as peripheral blood in humans, is a protein. Its expression was measured in human epidermal Keratinocytes. In a study involving rheumatoid arthritis patients, it was discovered that IL-17C expression was high in the blood.

The production of anti-IL17C antibody from chimeric human-mouse IgG2a antibody was used. The chimeric mouse-human IgG2a antibody was titrated against mouse IL17C with 100 nM in solution. Then, IL17C and the IL17 receptor E fusion protein were added to the Multi-array (r) 384-well plate Standard. The MSD Sector Imager 6000 measured the Streptavidin bindin assays.

Antibodies which recognize the IL17C molecule are antibody fragments as well as inhibitory nucleic acids and small organic compounds. These compounds include non-antibody compound molecules, such as ankyrin, fibronectin, and protein-derived molecules. Boster bio produces the best IL17C antibodies. This antibody can now be purchased online through antibodies-online GmbH located in Aachen.

Antibodies targeting IL17C have the potential to be very effective in the treatment of many respiratory disorders. In the case COPD IL-17C antagonists are highly effective in reducing inflammation. These compounds inhibit IL17C's recruitment to the lungs. They should be taken with other drugs. Patients suffering from COPD and bronchitis should have access to these antagonists.

IL-17C is also used in vaccines. It is a useful adjuvant for mucosal protection. It is used in multiple diseases such as psoriasis. The skin of mice that lack the gene IL-17C may also contain IL-17C. This could be used to help researchers create a better vaccine.