IDO1 Antibodies

Indoleamine 2,3-dioxygenase 1 (IDO1)

Catalyzes the first and rate limiting step of the catabolism of the essential amino acid tryptophan along the kynurenine pathway (PubMed:17671174). Involved in the peripheral immune tolerance, contributing to maintain homeostasis by preventing autoimmunity or immunopathology that would result from uncontrolled and overreacting immune responses (PubMed:25691885).

Tryptophan shortage inhibits T lymphocytes division and accumulation of tryptophan catabolites induces T-cell apoptosis and differentiation of regulatory T-cells (PubMed:25691885). Acts as a suppressor of anti-tumor immunity (PubMed:23103127, PubMed:25157255, PubMed:14502282, PubMed:25691885).

Gene Information

Human
Gene Name:	IDO1
Uniprot:	P14902
Entrez:	3620

Family

Belongs to:
indoleamine 2,3-dioxygenase family

Alternative Names

3dioxygenase; EC 1.13.11.52; IDO; IDO1; IDOIDO-1; INDO; INDOindole 2,3-dioxygenase; Indoleamine 2; indoleamine 2,3-dioxygenase 1; Indoleamine 2,3-dioxygenase; indoleamine-pyrrole 2,3 dioxygenase; Indoleamine-pyrrole 2,3-dioxygenase

Molecular Weight

Mass (kDA):
45.326 kDA

Genomic Context

Human
Location:	8p11.21
Sequence:	8; NC_000008.11 (39913891..39928790)

Tissue Specificity

Expressed in mature dendritic cells located in lymphoid organs (including lymph nodes, spleen, tonsils, Peyers's patches, the gut lamina propria, and the thymic medulla), in some epithelial cells of the female genital tract, as well as in endothelial cells of term placenta and in lung parenchyma (PubMed:25691885). Weakly or not expressed in most normal tissues, but mostly inducible in most tissues (PubMed:25691885). Expressed in more than 50% of tumors, either by tumoral, stromal, or endothelial cells (expression in tumor is associated with a worse clinical outcome) (PubMed:18418598). Not overexpressed in tumor- draining lymph nodes (PubMed:26155395, PubMed:25691885).

Subcellular Localizations

Cytoplasm, cytosol.

Diseases

• Malignant Neoplasms
• Neoplasms
• Inflammation
• Decreased Immunologic Activity [pe]
• Carcinoma
• Autoimmunity
• Infective Disorder
• Autoimmune Diseases
• Depressive Disorder
• Autoimmune Reaction
• Malignant Tumor Of Colon
• Chronic Inflammation

• Cell Transformation, Neoplastic
• Malignant Paraganglionic Neoplasm
• Tumor Escape
• Neoplasm Metastasis
• Crohn Disease
• Communicable Diseases
• Hiv Infections

Pathways

• Immune Response
• Cell Proliferation
• Pathogenesis
• Cell Activation
• T Cell Activation
• Cell Growth
• Vasodilation
• Cell Development
• Aging
• Response To Virus
• Adaptive Immune Response
• Localization
• Interleukin-10 Production

• Demethylation
• Methylation
• Decidualization
• Cell Cycle
• Cellular Localization
• T Cell Proliferation
• Biological Regulation

PTMs

• Acetylation
• Demethylation
• Nitration
• Phosphorylation

• Cleavage
• Methylation
• Oxidation
• Ubiquitination

Research Areas

• Cancer

For details, visit:
bosterbio.com/bosterbio-gene-info-cards/IDO1

Best Uses Of The IDO1 Marker

In this article, we will examine IDO1 activity assay kits that can be used to predict the value of IDO1 and its potential applications in cancer treatment. We will also examine the role IDO1 plays in graft-versus-host disease. Additionally, we will discuss the usefulness of IDO1 in combining several markers. This article will summarize the most recent research as well as its application to the treatment of cancer. This information is vital to the treatment of patients with advanced cancer.

IDO1 expression in tumor cells.

IDO1 is an enzyme that is activated in several human cancers. It is present in tumor cells, stromal cells and immune cells that are innate. The expression of this gene is associated with a poor prognosis. The enzyme blocks the activity of regulatory CD8+ cells and NK cells, as well as suppressing the effector cells of CD8+ T. It also functions as an interleukin 6 regulatory interface, shifting the inlammatory environment towards the development and promotion of new blood vessels.

The expression of this gene is tightly controlled in all kinds of cancers which include lung cancer as well as melanoma. In addition to cancer cells, it is expressed in endothelial and vascular cells and also in immune cells and stromal fibroblasts. At present, IDO expression is widely identified in cancer cell lines, as well as in various types of malignancies. The functions of IDO are not fully understood.

IDO expression is also associated with other immune-suppressive molecules. For example that, tumoral IDO is significantly related to the PD-L1 molecule, which regulates the immune response. In addition it has been observed that tumoral IDO expression suppresses anti-tumor reactions and increases the proliferation of human umbilical vein endothelial cells.

While IDO1 inhibitors have a long way to go, they may be able to combine IDO1 and IDO2 TDO inhibitions to dramatically extend the therapeutic range of many standard methods. It will likely continue to be the mainstay of cancer clinics for the next years. With the best combination of IDO1 inhibitors cancer clinics can expect to treat the disease with less chemotherapy sessions.

The IDO1 mRNA is expressed in various cancer cell types, including ovarian cancer and lung cancers that are adenosquamous. IDO1 expression is also connected to AhR signaling. The IDO-Kyn/AhR pathway triggers P27, which stimulates Kyn release in cancer cells. Metastatic growth requires the increase in TDO by tumor cells. In turn, genetic reduction of TDO reduces the invasiveness of the cells.

Although the function of IDO1 isn't fully understood yet, it plays an important function in the immune system. Small-molecule drugs are the best to attack IDO1 and its downstream effectsors as an intracellular target. Preclinical and clinical trials are in progress for a variety inhibitors. These compounds could be effective in transforming cancer cells. It may be time to think about a combination of TDO inhibitors and IDO1 inhibitors.

The IDO1 enzyme is a molecule that is controlled by tryptophan. A small molecules inhibitor of IDO1 blocks tryptophan biosynthesis. The IDO1 inhibitor BMS-986205 reduces the expression of tryptophan. TDO does not inhibit TDO, but can reduce the growth rate of tumor cells when it is used in conjunction with other hosts.

IDO1 kit for activity assay

Boster Bio IDO1 activity assay kit was developed to quantify IDO1 protein levels within cells. It has been tested by the Boster Bio laboratory. The test uses cell lysates of HCT 116 and HT-29 cells. The kit tests the concentration of Kyn to determine the activity of IDO1. To ensure the quality of the results, the assay was repeated three times.

In the laboratory, IDO1 expression is decreased in cancer cells. The cloned IDO1 sequence has been transfected into cells using the pmirGLO vector, which contains Renilla Luciferase, a reference reporter. IDO1 was transfected into 1x105 HT-299 or HCT116 cells and co-transfected (RiboBio China) with 40 miRNA NC and mimics. In cell lysates and lysates, Luciferase activities was measured for 24 hours after transfection. The Boster Bio IDO1 activity assay kit provides precise results.

The expression of IDO1 in colon cancer cells is connected to the expression of IFN-g. This protein reduces CD8+ T cells in response to antigens of the tumor. In the mouse model, IDO1 expression was associated with lower intratumoral C8+ cell infiltration. This suggests that IDO1 could be a part of an antagonistic feedback loop that regulates T cell activation. High IDO1 expression in patients with colon cancer did not correlate with overall survival. However IDO1 protein expression is high. IDO1 protein expression is positively and negatively related to colon cancer survival.

Boster Bio IDO1 Activity Assay Kit includes two reagents for detecting IDO1 or IDO2. The Antibody (PA1612) is a monoclonal rat anti-IDO1 antibody is the first. The antibody contains 5mg BSA and reacts with human INDOL1 (MLHFHYDTSNKIMEPHRPN).

IDO1 is expressed in various types of human cancers, and is especially frequent in colon cancer. However the antigen-antibody response to colon cancer could be weakened due to the effect of endogenous miRNAs. Furthermore, miR-448 was discovered to inhibit IDO1 expression, thereby limiting the function of CD8+ T cells in the tumor's microenvironment. This will enable the development of new immunotherapies by the detection of IDO1 activity in cancer cells.

The IDO1 Activity Assay Kit provides the results of IDO1 protein levels in the TME of various types of cancer. K-T is the ratio that determines the amount of IDO in the tissue. The ratio was higher in HDLEC supernatants that contain miR142-5p mimics and exosomes. The ratio of K-T did not change in NC samples. The K-T ratio is related to IDO levels of IDO.

Clinical studies on advanced CSCC patients validated the Boster Bio IDO1 activity assay kit. It also showed that there was a positive relationship with miR142-5p, which is circulating in the body. These two factors are believed to mediate the exhaustion of CD8+ T cell. IDO activity as well as cancer cells, could be a valuable target for CSCC. These data are not conclusive.

IDO1 expression in graft versus host disease

Recently, we found that IDO1 is a key regulator of cell growth in graft versus host disease. This study provides insight into the mechanism behind IDO1 transcription. It was discovered that miR153-3p is able to bind to IDO mRNA. This miRNA has multiple functions, including silencing gene expression and targeting specific genes. We have further studied the function of IDO1 using reporter plasmids.

To determine whether APCs play a crucial role in regulating IDO expression in GVHD we employed an animal model. We administered 200 mg of 3M-011 to B6 mice that had been lethally exposed to radiation. This caused transient expression in the colon of IDO. After 48 hours, the mice were killed and IDO mRNA levels were assessed. To examine the role of APCs in the graft versus host disease, we also utilized mice that were chimeric

The study also showed that IDO1 plays a role in causing damage to the gut. It ligates TLRs and triggers inflammation pathogenesis. This mechanism is not the only one to trigger IDO1 expression in GVHD. Another explanation could be the presence of other regulatory mechanisms. The IDO1 mRNA levels and the levels of proteins in the gut were significantly higher after graft-versus host disease.

This study proved that the presence of IDO in epithelial cells damps GVHD in a GCN2-independent fashion. In this study the expression of IDO1 in B6 BM of lethally irradiated mice resulted in the longer survival of IDO-/ chimeras compared to those with wt-IDO/ IDO-/ chimeras. It is difficult to prove that epithelial cells ' IDO production decreases the GVHD in a manner that can be measured in clinical situations.

We also looked into the effects of IDO1 on the PD-1 pathway regulators in the colon. We have already discussed that IDO1 expression is essential for T-cell tolerance development and could reduce the destructive cycle within the colon. These results are positive However, more research is needed to confirm these findings. However the research is restricted to APCs since they constitute only a small part of the colon.

Although the role of IDO in preventing aGVHD isn't fully understood but its upregulation has been implicated with immune tolerance. It has also been observed that IFN-g plays an important role in inducing IDO in the host during the GVHD response. In addition, miR146a can inhibit myeloprotection, autoimmunity, and cancer in mice. The authors concluded that these findings indicate the importance of IDO in the prevention and treatment of aGVHD.

The presence of miR-153-3p in the body suggests a role in aGVHD. There is still much to discover about how miR153-3p affects the IDO1 gene. Further research is required to determine if this molecule controls IDO during the last stages of host versus graft disease. It is currently up to investigate if miR-1533-3p regulates IDO in the later stages.