Human IL22 blocking peptide (CDBP1584)

Synthetic Human IL22 blocking peptide for BL

Product Overview
Blocking peptide for anti-IL-21 antibody
Species Reactivity
Application Notes
For in vitro research use only. Not intended for any diagnostic or therapeutic purpose. Not suitable for human or animal consumption.
200 μg/ml
50 μg
PBS containing 0.02% sodium azide
0.02% Sodium Azide
Store at -20℃, stable for one year.
UniProt ID
Antigen Description
IL22 (interleukin 22) is a protein-coding gene. Diseases associated with IL22 include chronic mucocutaneous candidiasis, and candidiasis, and among its related super-pathways are MIF Mediated Glucocorticoid Regulation and Regulation of eIF4 and p70S6K. GO annotations related to this gene include cytokine activity and interleukin-22 receptor binding.
cytokine activity; interleukin-22 receptor binding;
IL22; interleukin 22; interleukin-22; IL 10 related T cell derived inducible factor; IL 21; IL 22; IL D110; IL TIF; ILTIF; MGC79382; MGC79384; TIFa; TIFIL 23; zcyto18; cytokine Zcyto18; IL-10-related T-cell-derived inducible factor; IL-10-related T-cell-derived-inducible factor; IL-21; IL-22; IL-TIF; IL-D110; TIFIL-23;


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A Central Role for Lipocalin-2 in the Adaptation to Short-Bowel Syndrome Through Down-Regulation of IL22 in Mice


Authors: Zhang, Ailan; Sodhi, Chhinder P.; Wang, Menghan; Shores, Darla R.; Fulton, William; Prindle, Thomas; Brosten, Serena; O'Hare, Elizabeth; Lau, Alexander; Ding, Hua; Jia, Hongpeng; Lu, Peng; White, James R.; Hui, Justin; Sears, Cynthia L.; Hackam, David J.; Alaish, Samuel M.

BACKGROUND & AIMS: In short-bowel syndrome (SBS), inadequate intestinal adaptation is responsible for the majority of complications, including sepsis, liver failure, and death. In this study, we sought to further delineate the adaptive response to identify potential therapeutic targets. METHODS: We performed a 75% small-bowel resection (SBR) or sham operation on C57Bl/6J wild-type (WT), lipocalin-2 (LCN2)(-/-), and interleukin 22 (IL22)(-/-) mice. Exogenous IL22 was administered to SBR WT mice. Cecal fecal matter from SBR WT and SBR LCN2(-/-) mice were transplanted into germ-free mice. Intestinal permeability, inflammation, proliferation, and the microbiome were evaluated 1 week after surgery. CD4(+)IL22(+) laminal propria lymphocytes were sorted by flow cytometry. Naive T cells were polarized to T-helper cells with or without LCN2. RESULTS: A 75% SBR in a mouse re-creates the increased intestinal permeability, enterocyte proliferation, and intestinal dysbiosis seen in SBS. LCN2 expression increases after 75% SBR, and this increase can be abrogated with broad-spectrum antibiotic treatment. LCN2(-/-) mice have less intestinal inflammation, increased IL22 expression, and greater adaptation as evidenced by less intestinal permeability, increased carbohydrate enzyme expression, less weight loss, and less dysbiosis after 75% SBR thanWTmice. The proinflammatory and anti-adaptive effects of LCN2 can be transferred to germ-free mice via a fecal transplant. Administration of exogenous IL22 improves adaptation and restores the normal microbiome after 75% SBR in WT mice. CONCLUSIONS: LCN2 promotes inflammation and slows intestinal adaptation through changes in the microbiome and IL22 inhibition in a mouse SBS model. Strategies to reduce LCN2 may offer novel therapeutic approaches to enhance adaptation in SBS.

IL-22 Signaling Contributes to West Nile Encephalitis Pathogenesis


Authors: Wang, Penghua; Bai, Fengwei; Zenewicz, Lauren A.; Dai, Jianfeng; Gate, David; Cheng, Gong; Yang, Long; Qian, Feng; Yuan, Xiaoling; Montgomery, Ruth R.; Flavell, Richard A.; Town, Terrence; Fikrig, Erol

The Th17 cytokine, IL-22, regulates host immune responses to extracellular pathogens. Whether IL-22 plays a role in viral infection, however, is poorly understood. We report here that Il22(-/-) mice were more resistant to lethal West Nile virus (WNV) encephalitis, but had similar viral loads in the periphery compared to wild type (WT) mice. Viral loads, leukocyte infiltrates, proinflammatory cytokines and apoptotic cells in the central nervous system (CNS) of Il22(-/-) mice were also strikingly reduced. Further examination showed that Cxcr2, a chemokine receptor that plays a non-redundant role in mediating neutrophil migration, was significantly reduced in Il22(-/-) compared to WT leukocytes. Expression of Cxcr2 ligands, cxcl1 and cxcl5, was lower in Il22(-/-) brains than wild type mice. Correspondingly, neutrophil migration from the blood into the brain was attenuated following lethal WNV infection of Il22(-/-) mice. Our results suggest that IL-22 signaling exacerbates lethal WNV encephalitis likely by promoting WNV neuroinvasion.

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