Interleukin-17 receptor C Antibodies

Interleukin-17 receptor C (IL17RC)

Receptor for IL17A and IL17F homodimers as part of a heterodimeric complex with IL17RA (PubMed:16785495).

Receptor for the heterodimer formed by IL17A and IL17B as part of a heterodimeric complex with IL17RA (PubMed:18684971).

Has also been shown to be the cognate receptor for IL17F and to bind IL17A with high affinity with no need for IL17RA (PubMed:17911633). Activation of IL17RC contributes to induction of expression of inflammatory chemokines and cytokines like CXCL1 (PubMed:16785495).

Gene Information

Human
Gene Name:	IL17RC
Uniprot:	Q8NAC3
Entrez:	84818

Family

Belongs to:
No superfamily

Alternative Names

FLJ95963; FLJ96005; IL-17 RC; IL-17 receptor C; IL-17 RL; IL17F receptor; IL17RC; IL-17RC; IL17Rhom; IL17RL; IL-17RL; IL17-RL; interleukin 17 receptor C; interleukin-17 receptor C; Interleukin-17 receptor homolog; Interleukin-17 receptor-like protein; MGC10763; zcytoR14

Molecular Weight

Mass (kDA):
86.24 kDA

Genomic Context

Human
Location:	3p25.3|3p25.3-p24.1
Sequence:	3; NC_000003.12 (9917074..9933627)

Tissue Specificity

Expressed in prostate, skeletal muscle, kidney and placenta (at protein level) (PubMed:11706037). Expressed in brain, cartilage, colon, heart, intestine, kidney, liver, lung, muscle, placenta, and prostate (PubMed:11706037). Also detected in thyroid, trachea and adrenal gland (PubMed:17911633). Low expression in thymus and leukocytes (PubMed:11706037).

Subcellular Localizations

Cell membrane; Single-pass type I membrane protein. Soluble isoforms may be produced.

Diseases

• Malignant Neoplasms
• Inflammation
• Rheumatoid Arthritis
• Arthritis
• Prostatic Neoplasms
• Autoimmune Reaction
• Malignant Neoplasm Of Prostate
• Neoplasms, Hormone-dependent
• Neoplasms
• Adenocarcinoma
• Autoimmune Diseases
• Crohn Disease

• Autoimmunity
• Stomach Neoplasms
• Sclerosis
• Neoplasm Metastasis
• Adolescent Idiopathic Scoliosis
• Inflammatory Bowel Diseases

Pathways

• Secretion
• Pathogenesis
• Immune Response
• Intracellular Signal Transduction
• Rna Interference
• Chemokine Production
• Mitosis
• Dna Methylation
• Localization
• Cell Cycle Arrest
• Rna Splicing
• Methylation
• Chemotaxis

• Chemokine Secretion
• Mrna Transcription
• Translation
• Cell Cycle
• Regulation Of Mitosis
• Innate Immune Response
• Cell Growth

PTMs

• Methylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IL17RC

Best Uses Of The IL17RC Marker

Both the TCRb immunoseq r method and IL17RC mark are widely used to identify TCRb reactivity. TCRb immunoseq r (r) results showed that IL17RC antibodies were associated to a gradual decrease of host-reactive clones. The immunoseq method is a powerful tool for understanding the molecular basis of host-reactive clones.

TCRb-ImmunoSEQ(r), showed a gradual disappearance from host-reactive and clone clones

TCRb antibody in a 13-year old girl with fever, lymphadenopathy, sore throat and exudative symptoms was detected. The girl's imaging indicated that she had a peritonsillar cyst and was given antibiotics to treat the underlying infection. However, she became hypotension and thrombocytopenia worsening and eventually died. HSCTL-driven HLH was later diagnosed. Her immune phenotype, which included low naive T cells counts and an increase in BAFF, was similar to other children who had the same mutation.

TCRb ImmunoSEQ(r), performed by Boster Bio, showed a gradual disappearance of host-reacting clones. These clones could not be detected even after exogenous IL2 tests. This suggests that TCRb-based immunotherapy can reverse TCRb-mediated immunosuppression.

56 patients with TCRb related disorders were used in the study. These included children and adults. It found that 36% of patients with TCRb-associated lymphoma had host-reactive clones, but this was not the case with patients with primary immunodeficiency. Some patients with TCRb-related syndrome also showed abnormal humoral immunity, including hypogammaglobulinemia, poor vaccine-specific antibody responses, and hypogammaglobulinemia. Further, autoimmunity is more common in these patients than in the general population. These patients were also treated with immunosuppressants, IVIG, and a large number had the disease.

PID patients also had autoimmune symptoms in a subset. Patients with severe combined immune deficiency were diagnosed as having autoimmune cytopenia. 32 (16%) patients from the subgroup with phagocytic problems had autoimmune manifestations. The male-to–female ratio was 3:1. The most common autoimmune manifestations among these patients were autoimmune cytopenias and pyoderma gangrenosum.

The most common clinical manifestations were chronic diarrhea, pneumonia, skin infections, and failure of growth. Eight of the patients had multidrug-resistant tuberculosis. Patients treated with immunoglobulin therapy or hematopoietic cell transplantation were cured. The patient could use his right hand without limitations.

A genetic test for CXCR4 showed a positive correlation between the gene and the condition. The entire 124kb 6-SNP Haplotype with the super-enhancer that regulates CXCR4 expression within lymphocytes was the strongest risk factor. Moreover, paired RNA and genomic sequencing revealed a positive correlation between CXCR4 expression and sJIA risk.

IL17RC

The IL17RC cell-surface antigen receptor marker is expressed on T lymphocytes that have a unique phenotype. These cells are responsible to promote host defense diversity through acquiring a memory like phenotype. Researchers first identified nTh27 cell with mice models in 2009. Since then, they have expanded their studies to include additional species. The discovery of nTh27 cells led to a revolution in the Th2/Th2 paradigm, and the identification of IL-17A-producing cells facilitated the cloning of T-cells that express the IL-17RC marker.

T cells are a subset NK-cell cells that express IL17RC. The gene's promoter region is mapped to the CCR6 and CCR4 antigen receptors. This antigen is also known to promote the transcription of IL-17A via interaction with the rorc Gene. The IL17RC marker is a useful tool for the identification of T cells, which are the primary source of antibodies against Candida albicans.

T cells that are able to carry a GFP reporter can express the IL17RC genes. The gene is expressed in engineered mice, which only express the ligand IL-17A. In addition, mice lacking RORc do not generate Th27 cells and show reduced susceptibility to EAE. Th27 cells are lost when HIV is introduced to the body's membranes.

In addition, the IL17RC genetic has been linked to CCR6+-T-cells' production of IL-17A. This suggests that these cells are important contributors to the pathogenesis of HIV infection. The IL17RC genetic code is not yet well understood. It is important to understand the phenotypic, and functional roles of Th27-cells.

TCRb

Boster Bio, a biotechnology business, produces the IL17RC antibodies. It reacts to Human. It is stable at -20degC for up to a year and can be stored at 4degC for up to a month. The antibody is easily dissolved and there is a blocker peptide available for purchase. Cost depends on immunogen length. This antibody is approved for use in WB, IHC and ICC as well as ELISA.

TCRb ImmunoSEQ(r)

The IL17RC mark is an interleukin-1 receiver gene. The gene encodes a cytokine receptor protein. The IL17RC marker is a good choice for researchers looking to determine if this receptor is present in a particular tissue. However, the sensitivity of the IL17RC markers may be a key factor in determining the best use. Several methods are available for measuring the IL17RC marker in human tissue.