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We validate the specificity of these antibodies to Interleukin-22 by testing them on tissues known to express IL22 positively and negatively. Browse below to find the IL22 antibody that suites your experiment. We have 14 of these antibodies and many publications and validation images.
If you cannot find antibodies that fit your needs, contact us for making custom antibodies. We have a full suite of custom antibody services covering from research to diagnostic and therapeutic applications.
Facts about Interleukin-22.
Cytokine Zcyto18; IL-10-related T-cell-derived inducible factor; IL22; IL-22; IL-D110; IL-TIF; ILTIFIL-10-related T-cell-derived-inducible factor; IL-TIFMGC79382; interleukin 22; interleukin-22; MGC79384; TIFa; TIFIL-23; zcyto18
|Sequence:||12; NC_000012.12 (68248242..68253604, complement)|
If you're interested in learning about IL-22BP, IL-22, or both, you've come to the right place. In this article, you'll learn about the biology of these two molecules and their regulation. You'll also learn about how Boster scientists are utilizing these markers in their research. If you're a researcher looking for a way to test IL22 in your research, read on!
The discovery of IL-22BP has many implications. This protein regulates the levels of IL-22 cytokines in a complex range of tissues, including the skin, liver, GI tract, central nervous system, and brain. The dual nature of IL-22 and IL-22BP enables a greater understanding of the role of IL-22 in health and disease. The cytokine and its receptor, IL-22BP, are key players in inflammatory disease and immune homeostasis. Further studies are needed to fully understand IL-22BP's role in inflammatory disease and to determine its biological function.
IL-22BP plays a critical role in regulating the levels of IL-22 and IL-22BP in human cells. This cytokine is a potent regulator of many pathways within the body. IL-22BP is necessary for proper regulation of cytokine activity. IL-22BP regulates the activity of IL-22 after it is released by immune cells. Once secreted from the body, IL-22BP forms a 24-kDa protein that has two fibronectin-III domains in tandem.
Although the discovery of IL-22BP was initially focused on infectious diseases, it is now believed to have important roles in non-infectious inflammatory conditions. Inflammatory conditions such as asthma, fibrosis, and pulmonary disease can be exacerbated by the absence of IL-22BP, thereby increasing the risk of developing an infection. Moreover, IL-22BP regulates the bioactivity of IL-22 in lung tissues.
While IL-22BP is downregulated in the GI tract, it is important to note that it is expressed in inverse proportions in the colon of healthy mice. Inflammation and infection increase the level of IL-22BP, which has many functions in the GI tract. IL-22BP in Boster Bio enables a more targeted therapy for inflammatory diseases. In mice models of colitis, IL-22BP is inversely correlated with IL-22 in the colon.
IL22BP is a molecule that binds with greater affinity to IL-22 than the receptor. This makes it difficult for IL-22 to interact with the receptor on the cell surface and modulate signaling. IL-22 is a key cytokine in tissue responses to inflammation, particularly at barrier sites, such as the brain. IL-22BP controls the biological activity of IL-22 and may be useful in fighting infectious and chronic inflammatory diseases.
IL-22 is produced by CD4 T cells and group 3 innate lymphocytes. While it is primarily produced by these cells, other types of immune cells can also produce it. It is produced during an immune response, typically by a specific type of antigen. For CD4 T cells, this is a MHCII-presented peptide. In ILC3s, it is a part of a series of inflammatory proteins that regulate the immune system.
IL-22BP may be useful as a biomarker. Its ability to prevent IL-22 from activating cells may be useful in predicting outcome in colorectal cancer. For patients with active IBD, IL-22BP levels were undetectable. IL-22BP also reduces the production of mucin and antimicrobial peptides in the GI tract.
The IL22BP and IL-22BP are inversely regulated in healthy GI tissue. In healthy tissue, IL-22BP is present at lower levels than in inflammatory tissue. In contrast, IL-22BP is induced in CD4 T cells and ILC3 cells in mouse colitis models. Both proteins are upregulated in IBD and ulcerative colitis patients.
IL-22 is a dual-character hormone that has many sources and targets. While it plays an important role in tissue pathology and regeneration, it also has a potentially nefarious role in various human diseases. In the Boster Bio laboratory, we have discovered the complex biology of IL-22, and we'll discuss the potential clinical implications of the protein. This article will provide a brief overview of IL-22 biology.
IL-22 regulates cellular functions through signaling through a receptor complex, IL-22R1. IL-22R1 is found in human and murine kidney cells, where it activates downstream signal transduction pathways. In human cells, it promotes the phosphorylation of STAT3 and STAT5.
The Boster Bio Anti-IL-22 antibody is part of their Picoband(tm) catalog, and is tested in ELISA and WB applications. It's also stable at -20°C and can be stored for up to a year. Boster Bio Anti-IL-22 reacts with Mouse and Human IL-22 proteins. This antibody is made from recombinant human IL-22 protein.
The IL-22 gene is located on chromosome 12q15 near genes encoding IL-g and IL-26. It encodes a 179 amino acid protein with a 99% similarity to its mouse counterpart. It is active as a monomer in solution, but can form dimers when in high concentrations. It is also important to note that IL-22 is a cytokine and must be treated accordingly.
Inflammatory response to anti-CD40 therapy induced colitis, IL-22 was not effective. Inhibition of colitis by IL-22 may depend on its co-expression with other inflammatory cytokines. It also appears to be dependent on the presence of ILCs. There is no evidence that IL-22 directly induces colitis in humans. This inflammatory response, however, requires the involvement of ILCs.
The IL-22BP is a multi-functional protein that regulates several genes. Despite its homology with IL-22, it functions differently in different tissues. Its functions are largely dependent on the cellular environment. In this study, we examined the effect of IL-22BP on boster bio. After identifying its regulatory elements, we tested the IL-22BP-i2 in a Boster bio-derived cell line.
In the gut, IL-22BP regulates lipid adsorption by epithelial cells. Its decreased levels in the colon led to increased mucin levels and a decrease in Peyer's patches. Furthermore, mice lacking the IL-22BP gene showed reduced lipid adsorption, lower levels of enteric white adipose tissues, and a reduction in the accumulation of body fat.
IL-22BP binds to IL-22 with greater affinity than the cytokine itself. Without IL-22BP, IL-22 cannot interact with its cell surface-bound receptor and regulate cell signaling. IL-22BP regulates the biological activity of IL-22, a critical cytokine in tissue responses to inflammation, especially at barrier sites. Since IL-22BP regulates IL-22, it may have therapeutic value in chronic inflammatory diseases.
In contrast, IL-22BP expression in mouse colons was decreased in patients with UC or IBD. In the mouse IBD model, IL-22BP expression was decreased in CD4 T cells and TCRaKO mice. This pattern also applies to patients with ulcerative colitis. However, it is still unknown whether the increased IL-22BP expression was due to the inflammatory response to CD. This is an exciting study, which is worth pursuing.
The IL-22BP gene is responsible for inducing the expression of Muc in CECs, which are epithelial cells that line the colon. Interestingly, MucBP-Fc delivery also improves colitis symptoms in TCRaKO mice. In addition to improving colitis in these mice, IL-22BP-Fc has been shown to induce the expression of genes involved in the mucus layer.
IL-22BP inhibits the protective effects of IL-22 on epithelial cells in the colon. In patients with acute colitis, it inhibits the proinflammatory effect of IL-22. Nevertheless, despite its potential protective actions, there is still a great deal of uncertainty about how IL-22BP affects the intestine. Several studies have been conducted to understand the role of this cytokine.
The main source of IL-22BP is tumor infiltrated leukocytes (TILs). In a recent study, TILs were isolated and total RNA was used for cDNA synthesis. Real-time PCR revealed high expression of IL-22 in TILs and peripheral blood mononuclear cells. The authors also found no significant correlation between IL-22 expression and cancer-specific clinical characteristics.
Interestingly, IL-22BP is found to be increased in UC and CD lesions. Increasing numbers of these cells in inflamed mucosa may contribute to IL-22BP overproduction. Moreover, phenotypic analysis showed that a large proportion of IL-22BP+ cells in UC and CD were eosinophils. A few cells were HLA-DR+, but these were rare.
This research further indicates that IL-22BP is a dual role player in the development of colorectal cancer. In the early stages of the cancer model, IL-22 helps maintain the integrity of the barrier and reduces inflammation. However, in later stages, IL-22 promotes tumor growth, despite its protective effect. Therefore, mice lacking IL-22BP were more likely to develop colorectal cancer.
Nevertheless, IL-22BP inhibitory activity may be more relevant in the early phases of the disease. Moreover, in Il22ra2-/ rats, IL-22BP-deficient mice exhibited decreased susceptibility to acute colitis and a spleen-related inflammatory response. Further, IL-22BP-deficient rats exhibited a slowdown in disease progression compared with Il22ra2-/ littermates.
*More publications can be found for each product on its corresponding product page