IDO2 Antibodies

Indoleamine 2,3-dioxygenase 2 (IDO2)

Catalyzes the first and rate limiting step of the catabolism of the essential amino acid tryptophan along the kynurenine pathway (PubMed:17671174). Involved in immune regulation.

May not play a substantial role in tryptophan-related tumoral immunity (PubMed:25691885). .

Gene Information

Human
Gene Name:	IDO2
Uniprot:	Q6ZQW0
Entrez:	169355

Family

Belongs to:
indoleamine 2,3-dioxygenase family

Alternative Names

EC 1.13.11.-; IDO2; Ido-2; INDOL1; INDOL1indoleamine-pyrrole 2,3 dioxygenase-like 1; indoleamine 2,3-dioxygenase 2; Indoleamine 2,3-dioxygenase-2; indoleamine 2,3-dioxygenase-like 1 protein; Indoleamine 2,3-dioxygenase-like protein 1; Indoleamine-pyrrole 2,3-dioxygenase-like protein 1

Molecular Weight

Mass (kDA):
47.075 kDA

Genomic Context

Human
Location:	8p11.21
Sequence:	8; NC_000008.11 (39934955..40016391)

Tissue Specificity

Detected in liver, small intestine, spleen, placenta, thymus, lung, brain, kidney, and colon (PubMed:17671174). Also expressed at low level in testis and thyroid. Not expressed in the majority of human tumor samples (>99%) (PubMed:25691885).

Diseases

• Malignant Neoplasms
• Neoplasms
• Decreased Immunologic Activity [pe]
• Depressive Disorder
• Inflammation
• Carcinoma
• Renal Cell Carcinoma
• Malignant Paraganglionic Neoplasm
• Autoimmune Diseases
• Malignant Neoplasm Of Pancreas
• Cell Transformation, Neoplastic
• Autoimmune Reaction

• Neoplasm Metastasis
• Melanoma
• Pulmonary Embolism
• Malignant Tumor Of Colon
• Kidney Neoplasm
• Lung Diseases
• Lung Diseases, Obstructive

Pathways

• Cell Proliferation
• Translation
• Cell Activation
• T Cell Activation
• Immune Response
• Localization
• Senescence
• Stem Cell Proliferation
• Cellular Localization
• T Cell Proliferation

• Cell Growth
• T Cell Anergy
• Angiogenesis
• Pathogenesis
• Secretion

PTMs

• Phosphorylation

• Cleavage

• Acetylation

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IDO2

Best Uses Of The IDO2 Marker

This marker can be used to block autoreactive T and B cells by using a monoclonal antibody with high affinity. It can also be employed to target IDO2 via a therapeutic vaccination. Scientists are also able to submit their research for credit on the product. And, the best part is, these applications can be used by scientists around the world.

Monoclonal antibodies that target IDO2 block the autoreactive T and B cells activation by targeting it

Researchers previously discovered that targeting IDO1 or IDO2 with a monoclonally generated antibody slowed the activation of B and T cells that are autoreactive. However, this has been confirmed by the findings of the present study. The authors employed mice models to study whether these two enzymes are required for the activation of B cells. They used models of the influenza virus in mice infection and the type II model of immunization against antigens to study the importance of IDO1 and IDO2 in the activation of B cells.

IDO2 is also required for the normal development of B cells. Studies have demonstrated that KO mice have normal populations of B cells developing in bone Marrow, mature follicular cells in the spleen, and marginal zone B cells in the peritoneum. IDO1 Ko mice however have unaffected subpopulations B cells in the peritoneum.

Anti-CD8 T cells mAb targets IDO2 blocks autoeactive B and T cell activation in mice by blocking the IDO2 pathway. These cells do not have an antigen-presenting capability, however, mice who have IDO1 deletion have decreased antibody responses to stimuli that are either T cells-dependent or T-independent.

The mechanism for activation of T cells is complicated. First, T cells need to bind an antigen peptide on Class II MHC in order to activate macrophages. Second, CD40 secretion and IFNg secretion specifically target antigen-presenting macrophages. This process is slower than cytotoxicity mediated by CTL since the activation of macrophages depends on the binding of an antigen-presenting T cell.

A novel approach to treat autoimmune arthritis by targeting IDO2 with a monoclonally-produced monoclonal antibody. In preclinical models the monoclonal antibody slowed auto-reactive T and B cells activation, and helped reduce joint inflammation. This strategy highlights the enormous potential of antibody-mediated targeting of intracellular antigens to treat autoimmune diseases.

IDO2 inhibition is a better treatment than any of the other treatments for autoimmunity.

The mechanisms of IDO1 as well as IDO2 functions remains unclear. It is thought to mediate various cellular functions, including antimicrobial activity. Some studies have suggested that IDO2 could also regulate immune reactions and cause immunotolerance. More studies are required to identify the factors that influence IDO2 activity. IDO inhibition could be more effective than any of these treatments for autoimmunity.

IDO is expressed in synovial cells, which are often affected by autoimmune diseases. This is in line with immunosuppressive capability theory. IDO regulates excessive T-cell response. IDO inhibition however, can cause increased inflammation, tissue damage, and disease progression. Inhibiting IDO activity in human cells may also hinder the function of stem cells that promote autoimmunity.

Although it's not clear whether IDO2 interferes with the function of TDO but it could be more effective than either of the treatments. This enzyme is responsible for making l–Trp l–Kyn. It is capable of transforming regulatory T cells into Th-17-like types that release pro-inflammatory chemicals.

IDO2 is expressed in human tumor cells, but its role in autoimmune diseases is not known. However, it is highly expressed in certain tumors including non-small-cell lung cancer and pancreatic ductal adenocarcinoma. Furthermore, a gene known as Bin1 is not present in all human malignancies. This results to an increase in IDO expression. This phenomenon can be reversed by reducing IDO.

It is becoming increasingly clear that IDO plays a crucial role in the immune system. In a murine model, Uyttenhove et al. IDO inhibition significantly decreased T cell responses to tumors according to Uyttenhove and al. A study by Munn et al. Munn and colleagues. also discovered that inhibiting IDO2 reduced the Lymph nodes that drain cancerous cells. These results suggest that both IDO2 inhibition and anti-TNF treatment combined is more effective than either therapy alone.

IDO1 is much more than just an enzyme. It also plays an important role in the signaling pathway which profoundly alters immune cells' functional character. Recent crystallographic studies have revealed that IDO1 could have multiple binding modes which could result in distinct mechanisms of action. The indole-binding ring binds the catalytic pocket in the heme cofactor, yielding an trinary complex. When TGF-b is bound to DCs, Src homology 2 domain phosphatase-1 preferentially associates with the ITIMs.

Detecting IDO2 with a high-affinity main antibody

The ability to detect IDO2 with a monoclonal human antibody can be a powerful method to study the immune response to this protein. IDO2 is not the same as IDO1, but it has many distinct characteristics. It is essential for the regulation of T cells' differentiation and is involved in activation of B and T cells. In addition, it is associated with proinflammatory and tumorigenic effects. To determine if an antigen is able to detect IDO2 scientists must first determine its specificity.

Although IDO2 doesn't have to be present in all models, it is required in mice to regulate the response of antibodies. IDO2 double-ko mice exhibit decreased responses to type II antigens and influenza. These results indicate that IDO2 plays a key role in activating B cell and reducing the immune reaction to influenza. Nevertheless, there is no evidence that IDO2 directly suppresses the immune response.

Although IDO1 and IDO2 are both required for full B cell sensitivity However, the responses were not different in the laboratory. In fact, this could be due to the fact that IDO2 requires interactions with other immune system components. It is therefore possible that the stimulations applied in vitro can block the IDO2 pathway. However the presence of both IDO1 and IDO2 in the serum is critical for the identification of this protein.

IDO1 and IDO2 mRNA levels are very similar in mice. Additionally, both genes are required to ensure the proper development of B cells and for the production of IL-2. The use of high-affinity antibody to detect IDO1 will provide valuable insights into the immune system. This antibody can help researchers to determine the most important B cells that are involved in an immune response.

A high-affinity IDO2 primary antibody can be used to detect IDO2 in many different situations. In in vitro, ko as well as wt B cell responses to antigens as well as nonspecific antigens differ. TLRs, which act as sensors for immune cells are expressed on B-cells and are receptors on these cells. And, in addition to CD40 there are six other TLRs.

The detection of IDO2 is done using a low-background ELISA kit

A high-sensitivity, low background ELISA kit can detect IDO2 and help monitor the levels of this protein in blood of humans. This enzyme is closely linked to IDO1, and plays a part in the autoimmunity mediated by B cells. It also mediates activation of B and T cells and modulation of the immune system.

While IDO1 is implicated in immune responses however, its function in autoimmune disease isn't as than clear. While IDO1 is found in human B cells (human B cells) however, the levels of IDO1 in untreated B and T cells were lower than Western blotting detected. Additionally, IDO2 protein was absent in the dko mice, which do not have both the IDO1 and IDO2 protein.

In addition to the immune response initiated by B cells IDO2 produces proinflammatory effects on other types of cells. IDO1 acts as mediator in autoimmune processes and also influences T cells, whereas IDO2 acts directly on B cells. Studies have also shown that IDO2 is involved in normal B cell function. IDO2 ko mice show distinct phenotypic changes in the course of influenza and NP vaccination. For further confirmation double knockout mice are recommended to be used.

In vivo research has shown that IDO2 is necessary to ensure full cell responsiveness. However, B cells that express IDO2 are not as sensitive to antigens as B cells who express IDO1. This latter might be necessary to ensure proper function of B cells in the laboratory. In vitro studies showed that anti-IgM alone wasn't enough to detect differences in the immune response that are mediated by IDO1 or IDO2 in B cell.

In activated T cells as well as cells that were not activated, the levels of target and background proteins were determined. To assess the levels of these cells, the RNA was extracted from mice using a mini kit RNEasy from Qiagen. First strand cDNA was synthesized with oligo-dT-specific primers from Promega GoScript. The target gene was quantified by real-time PCR using SYBR Green. The relative expression level of IDO2 was determined as 2-(Ctb2M)-Cttargetgene).

For reliable results, it is important to select an ELISA kit that is reliable. To ensure that you get accurate concentration measurements, it's important to choose an ELISA kit with a standard curve with high-sensitivity. Be sure to read the datasheet and protocol booklet carefully when choosing the lowest background ELISA kit. To ensure reproducibility of the test, follow the recommended handling guidelines. The type of sample used and the dilution of the sample will determine the sensitivity of this method.