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GoPubMed Proteins lists recent and important papers and reviews for proteins. Page last changed on 19 Dec 2016.

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.
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.
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
Interleukin-17- and interleukin-22-secreting myelin-specific CD4(+) T cells resistant to corticoids are related with active brain lesions in multiple sclerosis patients.
Bento et al., Rio de Janeiro, Brazil. In Immunology, Feb 2016
Although the production of interleukin-6 (IL-6), granulocyte-macrophage colony-stimulating factor, IL-17 and IL-22 was less sensitive to hydrocortisone inhibition, only IL-17 and IL-22 levels correlated with active brain lesions.
Complementarity and redundancy of IL-22-producing innate lymphoid cells.
Vivier et al., Melbourne, Australia. In Nat Immunol, Feb 2016
Contrary to the prevailing view, we found by conditional deletion of the key ILC3 genes Stat3, Il22, Tbx21 and Mcl1 that NCR(+) ILC3 cells were redundant for the control of mouse colonic infection with Citrobacter rodentium in the presence of T cells.
Group 3 innate lymphoid cells continuously require the transcription factor GATA-3 after commitment.
Zhu et al., Bethesda, United States. In Nat Immunol, Feb 2016
Furthermore, GATA-3 was required for IL-22 production in both ILC3 subsets.
miRNA-Regulated Key Components of Cytokine Signaling Pathways and Inflammation in Rheumatoid Arthritis.
Chakraborty et al., Ch'unch'ŏn, South Korea. In Med Res Rev, Feb 2016
Moreover, we have tried to portray the role of various miRNAs in different cytokines such as TNF-α, IL-1, IL-6, IL-10, IL-17, IL-18, IL-21, and granulocyte macrophage colony-stimulating factor (GMCSF).
HIV and Tfh Cells: Circulating New Ideas to Identify and Protect.
Silvestri et al., Atlanta, United States. In Immunity, Feb 2016
(2016) report that circulating IL-21-producing CD4(+) T cells are phenotypically, transcriptionally, and functionally similar to lymphoid Tfh cells and that such HIV-specific Tfh cells were increased in RV144 trial vaccine recipients.
Recombinant lipidated dengue-3 envelope protein domain III stimulates broad immune responses in mice.
Chen et al., Taiwan. In Vaccine, Feb 2016
LD3ED III-immunized mice enhance wide ranges of T cell responses as indicated by IFN-γ, IL-17, IL-21 production.
Subclinical gut inflammation in ankylosing spondylitis.
Triolo et al., Palermo, Italy. In Curr Opin Rheumatol, Jan 2016
Furthermore, a growing body of evidence suggests that the gut of AS patients may be actively involved in the pathogenesis of AS through the production of proinflammatory cytokines, such as IL-23p19, and the differentiation of potentially pathogenic innate lymphoid cells producing IL-22 and IL-17.
Interleukin-22 promotes intestinal-stem-cell-mediated epithelial regeneration.
Hanash et al., New York City, United States. In Nature, Jan 2016
Using ex vivo organoid cultures, here we show that innate lymphoid cells (ILCs), potent producers of interleukin-22 (IL-22) after intestinal injury, increase the growth of mouse small intestine organoids in an IL-22-dependent fashion.
Hepatocytes: a key cell type for innate immunity.
Gao et al., Bethesda, United States. In Cell Mol Immunol, Jan 2016
interleukin (IL)-6, IL-22, IL-1β and tumor necrosis factor-α), and downstream signaling pathways (e.g.
Inflammaging and Anti-Inflammaging: The Role of Cytokines in Extreme Longevity.
Basile et al., Messina, Italy. In Arch Immunol Ther Exp (warsz), Jan 2016
We have described the role of IL-1, IL-2, IL-6, IL-12, IL-15, IL-18, IL-22, IL-23, TNF-α, IFN-γ as pro-inflammatory cytokines, of IL-1Ra, IL-4, IL-10, TGF-β1 as anti-inflammatory cytokines, and of lipoxin A4 and heat shock proteins as mediators of cytokines.
Halofuginone Treatment reduces interleukin-17A and ameliorates features of chronic lung allograft dysfunction in a mouse orthotopic lung transplant model.
Keshavjee et al., Toronto, Canada. In J Heart Lung Transplant, Jan 2016
Halofuginone treatment also decreased IL-17A and IL-22 transcripts at Day 14, transforming growth factor-β1 and matrix metalloproteinase-2 transcripts at Days 14 and 28.
Mycobacterium tuberculosis-Specific IL-21+IFN-γ+CD4+ T Cells Are Regulated by IL-12.
Wu et al., Guangzhou, China. In Plos One, Dec 2015
In the current study of Mycobacterium tuberculosis (MTB)-specific T and B cells, we found that MTB-specific peptides from early secreted antigenic target-6 (ESAT-6) and culture filtrate protein-10 (CFP-10) induced the expression of IL-21 predominantly in CD4+ T cells.
Interleukin-22 Alleviated Palmitate-Induced Endoplasmic Reticulum Stress in INS-1 Cells through Activation of Autophagy.
Zhang et al., Guangzhou, China. In Plos One, Dec 2015
Interleukin-22 (IL-22) plays a critical role in preventing β cells from oxidative and ER stress, and autophagy is associated with the survival and function of β cells.
An IL-23R/IL-22 Circuit Regulates Epithelial Serum Amyloid A to Promote Local Effector Th17 Responses.
Littman et al., New York City, United States. In Cell, Nov 2015
We identified an SFB-dependent role of type 3 innate lymphoid cells (ILC3), which secreted IL-22 that induced epithelial SAA production in a Stat3-dependent manner.
The importance of B cell-T cell interaction in autoimmune diseases.
Tanaka et al., In Nihon Rinsho Meneki Gakkai Kaishi, 2014
We assessed change of gene regulatory network that controls B cell differentiation after stimulation with BCR cross-linking, sCD40L, Toll-like Receptor (TLR) and cytokines such as IL-4/IL-21 in vitro.
Interleukin-22 protects intestinal stem cells from immune-mediated tissue damage and regulates sensitivity to graft versus host disease.
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.
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.
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.
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.
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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