TNFRSF13B Antibodies

Tumor necrosis factor receptor superfamily member 13B (TNFRSF13B)

Receptor for TNFSF13/APRIL and TNFSF13B/TALL1/BAFF/BLYS that binds both ligands with similar high affinity. Mediates calcineurin-dependent activation of NF-AT, along with activation of NF-kappa-B and AP-1.

Involved in the stimulation of B- and T- cell function and the regulation of humoral immunity. .

Gene Information

Human
Gene Name:	TNFRSF13B
Uniprot:	O14836
Entrez:	23495

Family

Belongs to:
No superfamily

Alternative Names

CD267 antigen; CD267; CVID; CVID2; FLJ39942; MGC133214; TACI; TACIMGC39952; TNFRSF13B; TNFRSF14B; Transmembrane activator and CAML interactor; tumor necrosis factor receptor 13B; tumor necrosis factor receptor superfamily member 13B; tumor necrosis factor receptor superfamily, member 13B

Molecular Weight

Mass (kDA):
31.816 kDA

Genomic Context

Human
Location:	17p11.2
Sequence:	17; NC_000017.11 (16939081..16972118, complement)

Tissue Specificity

Highly expressed in spleen, thymus, small intestine and peripheral blood leukocytes. Expressed in resting B- cells and activated T-cells, but not in resting T-cells.

Subcellular Localizations

Membrane; Single-pass type III membrane protein.

Diseases

• Immunologic Deficiency Syndromes
• Common Variable Immunodeficiency
• Autoimmune Reaction
• Autoimmune Diseases
• Autoimmunity
• Malignant Neoplasms
• Neoplasms
• Infective Disorder
• Immunoglobulin A Deficiency (disorder)
• Lupus Erythematosus, Systemic
• Lymphoma
• Multiple Myeloma
• Malignant Paraganglionic Neoplasm

• Primary Immune Deficiency Disorder
• Inflammation
• B-cell Lymphomas
• Rheumatoid Arthritis
• Arthritis
• Agammaglobulinemia
• Hyperplasia

Interacting Proteins

• MYD88
• SGTA
• TNFSF13B

Pathways

• Cell Maturation
• Pathogenesis
• Cell Activation
• Secretion
• Cell Proliferation
• Cell Differentiation
• B Cell Activation
• Immunoglobulin Production
• Cell Development
• B Cell Proliferation
• Isotype Switching
• B Cell Homeostasis
• Cell Growth

• Immune Response
• B Cell Differentiation
• Plasma Cell Differentiation
• T Cell Activation
• Cell Cycle
• Humoral Immune Response
• Localization

PTMs

• Phosphorylation

• Cleavage

• Ubiquitination

Research Areas

• Apoptosis
• Signal Transduction

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/TNFRSF13B

Best Uses of the TNFRSF13B Marker in CVID

This article will discuss TNFRSF13B which is a CVID related gene that is involved in the transcription "germ-line non-protein RNA transcripts". We will also talk about the ways in which Boster Bio uses this marker to test two patients who have an TNFRSF13B mutation. Whatever your research goals we hope this article was helpful.

TNFRSF13B, a CVID-related gene is

TNFRSF13B is a candidate for an underlying cause of disease, however the exact function of this gene in CVID is not known. The disease is characterized by a deficient immune system, leading to a high rate of infection with bacteria or viruses. People who have a CVID-associated gene are at risk of having recurrent infection, which can cause chronic lung diseases. People who suffer from CVID are also more likely to develop diarrhea and splenomegaly. Additionally, immune cells can be found in different organs.

Researchers sequenced the TNFRSF13B 5 exons of coding to find one mutation in nine patients. Incredibly, six patients had monoallelic TNFRSF13B mutations, however only one patient had biallelic mutation. A different group of 330 control subjects were also examined for sequence variants in the TNFRSF13B gene. Two of them were heterozygous for the C104R variant and one had an I87N allele. In healthy controls, there were no other missenses or biallelic mutations.

TNFRSF13B is a cell-surface receptor. It plays an important role in the immune system, supporting B-cell maturation. The gene's polymorphism has been maintained across a variety of mammalian species. This indicates that the gene's complicated properties are balanced , and help explain the mammalian's remarkable variety. For instance, TNFRSF13B may be thought to affect the production of T-independent antibodies by mice.

A recent study found that the expression of TACI is associated with higher plasma BAFF and decreased Treg frequency in CVID patients. These two effects, together with elevated levels of BAFF, may encourage the development of CVID. The higher levels of BAFF in CVID patients were significantly higher than in healthy individuals carrying the same TACI mutation. CVID-associated gene, TNFRSF13B, expression isn't enough to cause CVID. Instead, other susceptibility genes and nongenetic environmental factors are responsible for CVID-related illness.

TACI mutations interfere with the elimination of autoreactive cells from the central B cell tolerance checkpoint. TACI is also susceptible to defective TLR and BCR signals. However, TACI-related mutations may not enough to cause CVID They have been associated with an abnormal peripheral B-cell tolerance checkpoint. This is a significant discovery in immunology as well as the development of CVID.

It is involved in the transcription of non-protein-encoding "germ line" transcriptions of RNA

TNFRSF13B is a gene involved in the transcription of non-protein-encoding "gene line" RNA transcripts. This gene is activated by cytokines or specific activation signals. Activated TLRs, such as TNFRSF13B are responsible for causing these transcripts to form stable RNA-DNA hybrids their template DNA.

A new study has found a polymorphic allele of the TNFRSF13B gene that is associated with a higher risk of developing several cancer types. The study concluded that the polymorphism was in linkage equilibrium with another polymorphic allele. In silico analysis revealed that the SNP alters the sequence that is recognized by Neuron-Restrictive Silencing Factor, a gene associated with cancer. However, the mechanism between the allele and cancer is not clear.

TNFRSF13B is also involved in the production of MZ and B1 B cells, which respond to polysaccharides in the environment. These B cells can be activated through TNFRSF13B in a variety immune response processes. TNFRSF13B also plays a part in the transcription of non-protein-encoding "germline" RNA transcripts.

Autophagy is also influenced by TNFRSF10B gene. Inhibition of autophagy through pharmaceutical inhibitors or LC3B knockdown could cause autophagy to be inhibited, which may be an important molecular reason for HBV escape from TNFSF10 mediated antiviral immunity. This may be a contributing factor to chronic infections.

A higher risk of developing autoimmune disorders is linked to infections caused by TNFRSF13B. Researchers have discovered a variety new follicular Lymphoma genetic lesions. The gene encodes a mediator which limits the activation of T-cells. In addition, lymphoma B cells are antigen-presenting cells, and mutations in TNFRSF14 alter their capacity to trigger allogeneic T-cell responses.

DSBs are formed when short GC rich DNA sequences are combined. This happens in a sequential way, starting with VDJ sections of the IgH gene. Similar to the IgH locus, MMR recruits exonuclease 1, and other proteins, to the damaged ends. The DNA in the intervening region is removed or circularized. The nonhomologous repair of DNA machine joins the damaged junctions of the switch. It leads to the production of IgA an type of antibody.

It is utilized in Boster Bio.

TNFRSF13B is an immunogen that is used in boster bio. The body's immune system is controlled by the gene that codes TNFRSF13B. It is believed to be responsible for between 7% to 21 percent of CVID cases. CVID is the most prevalent type of primary immunodeficiency observed in the clinical setting. It is a heterogeneous illness characterised by the presence of antibodies. Patients suffering from CVID typically suffer from recurring respiratory infections and a high likelihood of developing autoimmune disorders like hemolytic anemia and thrombocytopenic purpura.

TNFRSF13B is also implicated in the development of inflammatory conditions, including CVID. CVID risk has been linked to the presence of polymorphisms in the TNFRSF13B gene. This includes the C104R variant and the variants A181E. The TNFRSF13B genetic variants are distinct genetic modifiers for the development of autoimmune diseases. The polymorphisms that occur in TNFRSF13B have a significant impact on the development of CVID.

It is used in two patients suffering from TNFRSF13B mutation

Boster Bio TNFRSF13B markers for the gene are chimeric allele-based tests that have been tested in two patients with TNFRSF-13B mutations. Two patients suffering from TNFRSF13B mutation have been able to test its sensitiveness and specificity. Both patients showed high-sensitivity to TNFRSF13B DNA. Both cases demonstrated that the mutations were associated with low or nonspecific cytotoxicity as well as poor vaccination response.

Both cases indicate that the TNFRSF13B polymorphisms C104R and A144E are associated with antibodies deficiency. However, their prevalence is not sufficient to rule out any transmission disequilibrium. In addition, patients who have TACI mutations experience decreased T-cell-independent responses to antigens, and mice that carry the A144E variant show impaired antibody responses.