Human Indoleamine 2,3-dioxygenase/IDO Antibody Summary
Accession # P14902
Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website.
Indoleamine 2,3‑dioxygenase/IDO in Human Tonsil. Indoleamine 2,3-dioxygenase/IDO was detected in immersion fixed paraffin-embedded sections of human tonsil using Mouse Anti-Human Indoleamine 2,3-dioxygenase/IDO Monoclonal Antibody (Catalog # MAB60301) at 1.7 µg/mL for 1 hour at room temperature followed by incubation with the Anti-Rabbit IgG VisUCyte™ HRP Polymer Antibody (Catalog # VC003). Before incubation with the primary antibody, tissue was subjected to heat-induced epitope retrieval using Antigen Retrieval Reagent-Basic (Catalog # CTS013). Tissue was stained using DAB (brown) and counterstained with hematoxylin (blue). Specific staining was localized to lymphocytes. View our protocol for IHC Staining with VisUCyte HRP Polymer Detection Reagents.
Preparation and Storage
- 12 months from date of receipt, -20 to -70 °C as supplied.
- 1 month, 2 to 8 °C under sterile conditions after reconstitution.
- 6 months, -20 to -70 °C under sterile conditions after reconstitution.
Background: Indoleamine 2,3-dioxygenase/IDO
Indoleamine 2,3-dioxygenase (IDO) is a heme-containing intracellular dioxygenase catalyzing the degradation of the essential amino acid L-tryptophan to N-formyl-kynurenine (1). This degradation is the first and rate-limiting step of the L-kynurenine pathway (2). IDO is widely expressed in dendritic cells, macrophages, microglia, eosinophils, fibroblasts, endothelial cells, and most tumor cells. In immune cells, its expression is mainly induced by cytokines such as IFN-gamma, IFN-alpha, IFN-beta, and IL‑10. IDO has an antimicrobial function due to its decreasing the availability of the essential amino acid tryptophan in inflammatory environments (3). Recent studies have demonstrated that IDO induces immunosuppression during infection, pregnancy, transplantation, autoimmunity, and neoplasia (3-5).
- Lewis-Ballester, A. et al. (2009) Proc. Natl. Acad. Sci. USA. 106:17371.
- Costantino, G. (2009) Expert Opin. Ther. Targets 13:247.
- Xu, H. et al. (2008) Immunol. Lett. 121:1.
- Lob, S. et al. (2009) Nat. Rev. Cancer 9:445.
- Curti, A. et al. (2009) Blood 113:2394.
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