Interleukin_21 _ IL21
- Known as:
- Interleukin_21 _ IL21
- Catalog number:
- GTX18496
- Product Quantity:
- 50 µg
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Interleukin_21 _ IL21
Related genes to: Interleukin_21 _ IL21
- Gene:
- IL21 NIH gene
- Name:
- interleukin 21
- Previous symbol:
- -
- Synonyms:
- Za11, IL-21
- Chromosome:
- 4q27
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-29
- Date modifiied:
- 2019-04-23
Related products to: Interleukin_21 _ IL21
Related articles to: Interleukin_21 _ IL21
- Elevated levels of the pro-inflammatory cytokine Interleukin 21 (IL-21) contribute to the progression of autoimmune and inflammatory diseases by binding to its receptor (IL-21R) and activating detrimental signaling pathways in immune cells. Consequently, we developed a recombinant decoy receptor protein designed to competitively inhibit IL-21 binding to its receptor. Using the extracellular domain of IL-21R as a scaffold, five key binding-site residues (33, 38, 70, 94, and 130) were mutated with OSPREY software. Computational analyses with GROMACS selected the Q33S, E38D, M70T, L94N, and M130S mutant for its superior structural stability and high binding affinity to IL-21, with binding energy calculations confirming that the mutant successfully maintains the high baseline binding affinity of the wild-type complex. The decoy receptor protein was subsequently expressed recombinantly in Rosetta-gami. More importantly, the analysis of secondary structure revealed that the protein retained its overall secondary structure after mutagenesis, with slight alterations in alpha-helical content. Finally, the calculation of the value using the SPR technique demonstrated that the mutant IL-21R exhibited a 1.4-fold increase in binding affinity compared to the wild-type receptor ( vs. for the wild-type), supporting its potential as a competitive IL-21R decoy receptor. Therefore, this decoy receptor could be considered an effective therapeutic agent for blocking IL21 and controlling or preventing the progression of autoimmune and inflammatory diseases. - Source: PubMed
Publication date: 2026/09/23
Vazifeshenas SaraHajihassan ZahraArab Seyed ShahriarNajafyar Ali - Cell motility, characterized by random walk and exploratory search movement, enables effector CD8+ T cells to search for sparse antigen-specific cancer targets within a tumor. This is of special relevance for treatment of solid cancers with adoptive T-cell receptor (TCR) T-cell therapy, where administered effector CD8+ T cells recognize specific MHC-I-presented antigens. Cell motility requires cytoskeleton remodeling to facilitate shape changes and movement. Herein, we show that increased mitochondrial Ca2+ levels are essential to reduce cytoskeleton stiffness of effector CD8+ T cells, leading to acquisition of a polarized shape and high motility. IL-21, but not IL-7 or IL-15, was able to raise mitochondrial Ca2+ levels in effector CD8+ T cells and increase their motility without affecting survival and proliferation. This increase in mitochondrial Ca2+ levels triggered by IL-21 was driven by sustaining mitochondrial membrane potential through mitochondrial STAT3, independently of its transcriptional activity. Enhanced motility of effector CD8+ T cells led to a superior killing efficacy of antigen-specific melanoma cells in vitro. Furthermore, enhanced mitochondrial Ca2+-mediated motility of adoptive TCR-specific effector CD8+ T cells resulted in a superior antitumor efficacy of this treatment against solid tumors in vivo. Thus, enhancing effector CD8+ T-cell motility is a promising strategy to boost efficacy of adoptive T-cell therapies against solid tumors. - Source: PubMed
Publication date: 2026/09/21
Hoen Rauhut MaureenAbdullahi FahiimaWalters JayPatel Hiten NStich DominikMarié Isabelle JWen HaitaoLevy David EJacot Jeffrey GJacobelli JordanValenca-Pereira FelipeRincon Mercedes - Cancer-associated fibroblasts (CAFs) have been recognized as key contributors to tumor progression. Chimeric antigen receptor (CAR) T-cell therapy targeting fibroblast activation protein (FAP), a marker of CAFs, has gained attention and is being evaluated in both preclinical and clinical studies. Cord blood (CB)-derived CAR natural killer (NK) cell therapy has shown efficacy in hematologic malignancies. In this study, we generated FAP-targeting CAR NK cells (FAP-CAR NK cells). CD3-depleted CB mononuclear cells were stimulated with irradiated K562 cells expressing 4-1BB ligand (tumor necrosis factor ligand superfamily member 9) and membrane-bound interleukin-15 and interleukin-21 to expand NK cells, into which FAP-CAR was introduced. FAP-CAR NK cells produced cytokines and exerted cytotoxic activity when co-cultured with FAP-transduced HT1080 cells and CAFs isolated from human lung cancer tissue. In a xenograft model established by intrathoracic co-injection of A549 lung cancer cells and luciferase-expressing CAFs, injection of FAP-CAR NK cells, but not control CD19-CAR NK cells, resulted in their robust expansion and persistence in vivo for 5 weeks. However, CAFs were not eliminated by FAP-CAR NK cells, although CAR NK cells were clearly detected in the tumors. The levels of cytotoxicity-associated molecules (such as granzymes) were higher in FAP-CAR NK cells persisting in the spleens of mice compared with those in pre-infusion FAP-CAR NK cells. These results indicate that FAP-CAR NK cells have the potential to respond specifically to the target antigen and expand robustly in vivo, although further optimization is required to maintain cytotoxic function for a prolonged duration in vivo. - Source: PubMed
Publication date: 2026/09/20
Hiroshima TakashiKimura ToruMaekawa MarikoNoguchi MayukoMatsui TakahiroIkeda ShunyaSuga MakikoNagata HidekiKimura KenjiFukui ErikoKanou TakashiOse NaokoMorii EiichiShintani YasushiHosen Naoki - Cell-based immunotherapies of PBMC-derive Natural killer (NK) cells have demonstrated substantial potential for the treatment of hematologic malignancies. However, its application is limited due to the complex and inefficient gene modification and the insufficient therapeutic efficacy against solid tumors . - Source: PubMed
Publication date: 2026/09/03
Li YangyangWang YehaiZhang XimengFan YanPan LinaWu JingXiao Weihua - Spotty Liver Disease (SLD) is an acute bacterial infection of layer chickens in production, caused by Campylobacter hepaticus, and occurs most frequently in barn-housed and free-range systems. The disease is characterized by a sharp decline in egg production and increased mortality. The hallmark pathological feature is 1-2 mm white to grey necrotic foci distributed across the liver surface. Despite its growing economic impact on commercial poultry, the molecular mechanisms underlying host responses to C. hepaticus infection remain poorly understood. To address this gap, we performed a comprehensive transcriptome analysis of liver tissue from chickens naturally infected with SLD compared to uninfected controls. Illumina NovaSeq-based RNA sequencing was performed on liver tissues collected from three SLD-infected and three uninfected control chickens, with three biological samples for each sample type (n = 6), yielding 9,277 differentially expressed genes (DEGs), of which 3,063 were upregulated and 6,214 were downregulated. Functional pathway enrichment analysis revealed significant alterations in immune and metabolic processes associated with SLD pathophysiology. Infected chickens exhibited significant activation of immune response pathways, particularly cytokine-cytokine receptor interactions involving interleukins IL-22, IL-21, and IL-6, along with enhanced cell signaling, and cell adhesion. Among the individual genes, C1QTNF1 and the adhesion molecule gene ADGRD1 were notably overexpressed, indicating enhanced inflammatory activity. In contrast, core hepatic metabolic functions were profoundly reduced (adjusted p < 0.05) as evidenced by downregulation of oxidative phosphorylation, fatty acid metabolism, iron ion binding, and heme binding pathways. A marked increase in serum amyloid A (SAA) gene expression further indicated robust acute-phase responses and compromised liver function during infection. Together, these findings demonstrate a complex interplay between inflammatory activation and metabolic dysregulation during SLD. The strong upregulation of acute-phase proteins and pro-inflammatory cytokines demonstrates the host's vigorous attempt to combat bacterial infection, whereas the concurrent suppression of essential metabolic pathways reflects the pathological consequences of SLD. This study provides a transcriptomic characterization of host responses to C. hepaticus infection, offering insights into SLD pathogenesis and potential avenues for targeted intervention. - Source: PubMed
Publication date: 2026/09/16
Bommineni VarshaEdison Lekshmi KGottapu ChaitanyaButcher Gary DKariyawasam Subhashinie