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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 27 Nov 2014.

Interleukin 21

IL-21, IL-22, Interleukin-21, interleukin-22
This gene encodes a member of the common-gamma chain family of cytokines with immunoregulatory activity. The encoded protein plays a role in both the innate and adaptive immune responses by inducing the differentiation, proliferation and activity of multiple target cells including macrophages, natural killer cells, B cells and cytotoxic T cells. Dysregulation of this gene plays a role in multiple immune-mediated diseases including lupus, psoriasis and chronic inflammatory diseases. Alternatively spliced transcript variants encoding multiple isoforms have been observed for this gene. [provided by RefSeq, Dec 2011] (from NCBI)
Top mentioned proteins: IL-17, CD4, Interleukin-6, CAN, IL-10
Papers using IL-21 antibodies
The biology of human natural killer-cell subsets.
Supplier
Sandberg Johan K., In PLoS ONE, 2000
... IL-7, IL-4, IL-9; 50 ug/mL IL-12, 0.25 mg/mL IL-18 (all from R&D Systems); 100 ug/mL IL-21 (Miltenyi Biotec), 5 ug/mL IL-15 (PeproTech), 100 ...
Modulation of flagellar expression in Escherichia coli by acetyl phosphate and the osmoregulator OmpR.
Supplier
Masucci Maria G., In PLoS ONE, 1994
... Cells were stimulated with human recombinant IL-22 (Cell Signaling Technologies) for the indicated ...
Papers on IL-21
The Immunopathogenesis of Psoriasis.
Review
New
Krueger et al., New York City, United States. In Dermatol Clin, 31 Dec 2014
Most of the psoriatic T cells discretely produce interferon-γ, interleukin (IL)-17, and IL-22.
Inhibitors of phosphodiesterase 4 (PDE 4): a new therapeutic option in the treatment of psoriasis vulgaris and psoriatic arthritis.
New
Adamski et al., Poznań, Poland. In J Dermatolog Treat, 26 Dec 2014
UNLABELLED: Abstract Psoriasis vulgaris (PV) and psoriatic arthritis (PsA) are inflammatory diseases in which inflammation and sustained inducing lesions result from immune disorders associated with overactivity of T cells that produce multiple proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α) and interleukin: IL-2, IL-12, IL-17, IL-22 or IL-23.
The IL-20 subfamily of cytokines - from host defence to tissue homeostasis.
New
Impact
Ouyang et al., San Francisco, United States. In Nat Rev Immunol, 25 Dec 2014
The interleukin-20 (IL-20) subfamily of cytokines comprises IL-19, IL-20, IL-22, IL-24 and IL-26.
A High Frequency of Peripheral Blood IL-22(+) CD4(+) T Cells in Patients With New Onset Type 2 Diabetes Mellitus.
New
Jiang et al., Changchun, China. In J Clin Lab Anal, 25 Dec 2014
BACKGROUND: This study is aimed at investigating the frequency of different functional IL-22(+) CD4(+) T cells in Chinese patients with type 2 diabetes mellitus (T2DM).
Activation of the Interleukin-34 Inflammatory Pathway in Response to Influenza A Virus Infection.
New
Liu et al., Wuhan, China. In Am J Med Sci, 20 Dec 2014
The expression level of IL-34 in IAV-infected PBMCs was blocked by IL-22-specific siRNA.
Role of interleukin-21 in HBV infection: friend or foe?
Review
New
Hou et al., Guangzhou, China. In Cell Mol Immunol, 03 Dec 2014
The roles of IL-21 in modulating immunity to infections are currently being defined.
Glycemic control in diabetes is restored by therapeutic manipulation of cytokines that regulate beta cell stress.
New
Impact
McGuckin et al., Brisbane, Australia. In Nat Med, 02 Dec 2014
In obese mice, antibody neutralization of IL-23 or IL-24 partially reduced beta cell ER stress and improved glucose tolerance, whereas IL-22 administration modulated oxidative stress regulatory genes in islets, suppressed ER stress and inflammation, promoted secretion of high-quality efficacious insulin and fully restored glucose homeostasis followed by restitution of insulin sensitivity.
[The changes of circulating follicular regulatory T cells and follicular T helper cells in children immune thrombocytopenia].
New
Guo et al., Zhengzhou, China. In Zhonghua Xue Ye Xue Za Zhi, 30 Nov 2014
The proportion of circulating Tfr and Tfh cells were determined by flow cytometry; real-time PCR was performed to detect the expression of transcription factors and regulatory factors of Bcl-6, c-Maf, Blimp-1 and PD-1 mRNA; ELISA was used to detect plasma concentration of IL-2, IL-6, IL-10 and IL-21.
The Necroptosis Adaptor RIPK3 Promotes Injury-Induced Cytokine Expression and Tissue Repair.
New
Impact
Chan et al., Worcester, United States. In Immunity, 16 Nov 2014
Ripk3(-/-) mice exhibited an impaired axis of injury-induced IL-1β, IL-23, and IL-22 cytokine cascade, which was partially corrected by adoptive transfer of wild-type DCs, but not Ripk3(-/-) DCs.
Interleukin-22 Regulates the Complement System to Promote Resistance against Pathobionts after Pathogen-Induced Intestinal Damage.
New
Impact
Inohara et al., Ann Arbor, United States. In Immunity, 16 Nov 2014
Here, we report a critical role for interleukin-22 (IL-22) in systemic protection against bacterial pathobionts that translocate into the circulation after infection with the pathogen Clostridium difficile.
Complement and IL-22: Partnering Up for Border Patrol.
New
Impact
Kemper et al., London, United Kingdom. In Immunity, 16 Nov 2014
(2014) show that the host's protective measures against such events include interleukin-22-driven systemic elimination of pathobionts via complement regulation.
Interleukin-17 in human inflammatory diseases.
Review
New
Shahneh et al., Tehrān, Iran. In Postepy Dermatol Alergol, Aug 2014
Human Th17 pro-inflammatory cells are currently defined as cells that produce IL-17A and F, tumor necrosis factor (TNF)-α, IL-6, IL-21, IL-22 and IL-23.
Interleukins in chronic liver disease: lessons learned from experimental mouse models.
Review
New
Tacke et al., Aachen, Germany. In Clin Exp Gastroenterol, Dec 2013
IL-22, on the other hand, protects from development of fibrosis or steatohepatitis.
Utilizing cytokines to function-enable human NK cells for the immunotherapy of cancer.
Review
New
Fehniger et al., Saint Louis, United States. In Scientifica (cairo), Dec 2013
Here, we review the roles of major cytokines that regulate human NK cell development, survival, and function, including IL-2, IL-12, IL-15, IL-18, and IL-21, and their translation to the clinic as immunotherapy agents.
Exclusion of IL-21 in the pathogenesis of OVA-induced asthma in mice.
New
Xiong et al., Wuhan, China. In Int J Clin Exp Med, Dec 2013
IL-21 has a variety of effects on the immune system.
Interleukin-22 protects intestinal stem cells from immune-mediated tissue damage and regulates sensitivity to graft versus host disease.
Impact
GeneRIF
van den Brink et al., New York City, United States. In Immunity, 2012
IL-22 as a critical regulator of tissue sensitivity to GVHD and a protective factor for intestinal stem cells during inflammatory intestinal damage.
Preparation and characterization of mouse IL-22 and its four single-amino-acid muteins that act as IL-22 receptor-1 antagonists.
GeneRIF
Gertler et al., Israel. In Protein Eng Des Sel, 2012
Recombinant mouse il-22 (mIL-22) and its variants were expressed in E coli, refolded and purified.The binding of IL-22 and its four muteins to immobilized mIL-22 receptor alpha1 extracellular domain (mIL-22 Ralpha1-ECD) exhibited similar affinity.
NK1.1+ cells and IL-22 regulate vaccine-induced protective immunity against challenge with Mycobacterium tuberculosis.
GeneRIF
Vankayalapati et al., Tyler, United States. In J Immunol, 2012
IL-22, produced by NK1.1-expressing cells, induces optimal protective immunity through enhancing antigen-specific T cell responses after challenge with Mycobacterium tuberculosis.
IL-21 promotes lupus-like disease in chronic graft-versus-host disease through both CD4 T cell- and B cell-intrinsic mechanisms.
GeneRIF
Rus et al., Baltimore, United States. In J Immunol, 2012
IL-21 promotes autoimmunity in chronic graft-versus-host disease through both CD4+ T cell- and B cell-intrinsic mechanisms.
Activated and resting regulatory T cell exhaustion concurs with high levels of interleukin-22 expression in systemic sclerosis lesions.
GeneRIF
Gorochov et al., Paris, France. In Ann Rheum Dis, 2012
Systemic sclerosis pathogenesis does not appear to be linked to IL-17-, but rather to IL-22-producing cells with skin-homing potential and a concomitant quantitative Treg defect.
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