Interleukin-17 receptor B Antibodies

Interleukin-17 receptor B (Il17rb)

Receptor for the proinflammatory cytokines IL17B and IL17E.

May play a role in controlling the development and/or differentiation of hematopoietic cells.

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Gene Information

Mouse
Gene Name:	Il17rb
Uniprot:	Q9JIP3
Entrez:	50905

Family

Belongs to:
No superfamily

Alternative Names

CRL4IL-17 receptor homolog 1; cytokine receptor CRL4; Cytokine receptor-like 4; Evi27; EVI27IL-17B receptor; IL-17 RB; IL-17 receptor B; IL-17 RH1; IL17BRinterleukin 17B receptor; IL-17ER; IL17RB; IL-17RB; IL17Rh1; IL-17Rh1; IL17RH1MGC5245; interleukin 17 receptor B; interleukin 17 receptor homolog 1; interleukin-17 receptor B; Interleukin-17B receptor

Molecular Weight

Mass (kDA):
55.617 kDA

Genomic Context

Mouse
Location:	14 B|14 18.39 cM
Sequence:	14;

Tissue Specificity

Liver and testis. Expressed at lower level in kidney and lung. Expressed in selected T-cell, B-cell and myeloid cell lines.

Diseases

• Malignant Neoplasms
• Mammary Neoplasms
• Malignant Neoplasm Of Breast
• Inflammation
• Neoplasms
• Asthma
• Neoplasm Recurrence, Local
• Lung Diseases
• Neoplasm Invasiveness
• Early-stage Breast Carcinoma
• Autoimmune Diseases
• Rhinorrhea
• Allergy

• Hay Fever
• Eosinophilia
• Atherosclerosis
• Pneumonia
• Allergic Rhinitis (disorder)
• Autoimmune Reaction
• Cholangiocarcinoma

Pathways

• Cytokine Production
• Pathogenesis
• Methylation
• Reverse Transcription
• Chemokine Production
• Tissue Remodeling
• S Phase

• Dna Methylation
• Secretion

PTMs

• Glycoprotein

Research Areas

• Cytokine Research

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/Il17rb

Boster Bio: Best Uses Of The IL-17RB Marker

We'll be talking about IL-17RB (a cytokine responsible for controlling inflammation and pancreatic tumors) in this article. We'll be discussing the high-affinity secondary antibodies available for this gene as well as how these could lead to new drug development. The IL-17RB mark is a highly cited marker in immunohistochemistry.

IL-17RB regulates inflammation.

The cytokine IL-17RB has also been identified as a part of the IL-17 Family. The receptor subunits consist of single transmembrane chain chains that have an extracellular domain called FN III. The receptor subunits have a cytoplasmic motif that is similar in appearance to the Toll/IL-1R region homologous. The receptor subunits have the ability to transduce a similar signal and activate an adaptor protein known as nuclear factor-kappaB activater 1.

IL-17B activity depends on the IL-17RB receptor and the IL-17RB Subunit. The IL-17RA cytokine subunit is essential for IL-17B to convert signals to other cytokines. Both subunits have been found to be ubiquitously expressed. They are responsible to regulate inflammation as well as host defense. Further, the subunits of IL-17RB are important for immune system function and autoimmune disease.

The IL-17R complex consists of two molecules, IL-17RA (or IL-17RD). These two molecules regulate inflammation through binding to the IL-17A/IL-17F heterodimers. Skin keratinocytes produce IL-17RA. It plays a critical role in IL-17-dependent skin inflammation. It regulates inflammation in skin.

IL-17A is a cytokine that is associated with early lung fibrosis and inflammation. It regulates expression of proinflammatory cytokines as well as chemokines throughout the BLM including IL-8. IL-17A is also involved in the inflammatory response and the epithelial-mesenchymal transition, all of which contribute to fibrosis.

IL-17A, the main effector molecule in psoriasis, is responsible. It stimulates human umbilical vein epithelial cells to make IL-8. Moreover IL-17D can suppress the production and proliferation of myeloid cells. These findings indicate that IL-17A is directly involved in regulating hematopoietic response to inflammation.

Both IL-17A/IL-17C are essential for pulmonary fibrosis. Cascade signaling plays a critical role in IPF progression through IL-17A/IL-17B. IL-17D, IL-17E, and IL-17E both play important roles in inflammatory responses but are not directly related to IPF.

An unknown trigger is believed to cause pathogenic Th27 cancer cells. Myeloid cells produce Th27 polarizing cytokines, which trigger inflammation. These cells then travel back and activate keratinocytes. Keratinocytes respond by releasing inflammatory mediators. However, IL-17E/IL-17RB do not have a direct relationship to psoriasis.

It acts as a regulator for pancreatic carcinoma

The progression and spread of aggressive pancreatic tumors is linked to the expression IL-17RB. In a mouse xenograft experiment, neutralizing antibodies against IL-17RB protein reduced tumor growth and tumor metastasis. These findings reveal a new therapeutic target to treat pancreatic tumors and suggest that this receptor may play a significant role in the progression of the disease.

The progression and metastasis of pancreatic carcinoma can be caused by the overexpression or partial absence of IL-17B. This receptor is also associated with survival and progression-free survival, which provide insight into a potential therapeutic target. Although there is still much to be done, the results are encouraging. The authors concluded that IL-17RB regulates pancreatic disease. Further studies will be required in order to determine the impact of IL-17RB on pancreatic cancer progression.

The Chinese Medical University team discovered IL-17RB's role in tumor development. Researchers developed a synthetic peptide which blocks IL-17RB signals. The peptide might also be used in the treatment of other cancers that are influenced via the IL-17RB pathway. These studies suggest that inhibitors may be a therapy for pancreatic disease.

Tumorigenesis is thought to be caused by IL-17B or IL-17RB. It is believed that IL-17RB regulates expression of inflammatory chemicals. It is not yet clear what mechanism IL-17RB uses to promote tumor growth. However, patients with pancreatic tumors were found to have a lower survival rate and had less success when they had higher levels. Also, mice with high levels of this protein had higher tumor formation.

It has been also shown that patients with a lower prognosis are more likely to have a high phosphorylated IL-17RB level. Loss of RB function results in a significant increase of activated Ras. Moreover, a loss in RB activity can cause the expression NFB activator 1, a downstream signaling factor for cancer cells. Pancreatic cancer can be prevented by blocking this pathway.

It is a target of high-affinity primary antibody

IL-17RB is a subunit of the interleukin-receptor that binds with IL-17B. It plays a key role in bone formation and inflammation. IL-17B is a pro-inflammatory cytokine that can be bound to IL-17 RB. It also induces the infiltration and production of inflammatory immune cells. IL-17RB is overexpressed in aggressive breast cancer cell lines, and its overexpression promotes tumorigenicity.

High-affinity primary antibodies are designed to recognize IL17RB by binding to a specific epitope on the surface of a protein in fixed tissues. This high-affinity antibody can make it more difficult to extract the antibodies from the columns. Additionally, elution from the column can be difficult, requiring harsh or denaturing techniques.

IL-17RB plays a vital role in the immune system. It is also involved as an allergen and in atopy. It is therefore important that anti-inflammatory antibodies target the receptor. These can also target a variety of cellular targets. These include IL-17RB/IL-25 and IL17.

A cell culture technique was developed to determine if IL17RB is a viable target. The cells were enriched in CD4+CRTH2T cell-derived T cells using a CD4+T Cell Isolation Kit. The cells were stained with anti CD3 FITC and anti-CD28 antibodies and sorted on a FACSAria flowcytometer.

IL17RB belongs to the interleukin-1 family. It binds CXCR1 as well as CXCR2 receptors. Its presence in hematopoietic stem, progenitor and progenitor cell lines suggests that it may be involved in the development chronic myeloid leukemia. This target could help improve the management of many diseases, including rheumatoid.

Although the target of IL17RB remains unknown, high-affinity primary antibody targeting it may be able block tumor growth by increasing the binding affinity of these antibodies to its target. The increased affinity may result in anti-tumor and cancer mAbs being more effective. CD16A has also been identified as a promising candidate in the development of cancer cell therapies.

It could spark drug development

Boster Bio IL17RB, a novel marker for IL17RB, has been discovered. This discovery could lead to new drug development in the area of cancer. The IL17RB pathway regulates inflammation. In some diseases, its inhibitory action has been associated with the growth and progression in certain types. A peptide, similar to the IL17RB antagonist used in the study, could also be used to treat breast or pancreatic cancers, two conditions where IL-17RB plays a critical role.