Interleukin_21 _ IL21
- Known as:
- Interleukin_21 _ IL21
- Catalog number:
- AP09162PU-S
- Product Quantity:
- 25 µl
- Category:
- -
- Supplier:
- ACR
- Gene target:
- Interleukin_21 _ IL21
Ask about this productRelated 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
- Cytokines used during chimeric antigen receptor (CAR) T-cell manufacturing can influence product differentiation and functional fitness. - Source: PubMed
Publication date: 2026/08/25
Val-Casals MariaAltuna AnePérez-Amill LorenaArmand-Ugón MercedesPeña SergioLópez-Pecino AnaColomer DolorsEsteve JordiJuan ManelKlein-González Nela - Chronic periodontitis (CP) is an inflammatory-destructive disease, and Th17 cells play a vital role in driving and regulating CP. This study aimed to confirm the influence of miR-3917/HLA-DRB1 in the differentiation of CD4 T cells to Th17 cells. The differentially expressed microRNAs (miRNAs) in CP were screened from the Gene Expression Omnibus (GEO) database, and then the target gene of miR-3917 was confirmed by using the RT-qPCR and Dual-Luciferase assay. clinical data of patients with CP and healthy individuals were collected, and intergroup comparisons were performed using ROC and logistic regression analysis. A CD4T cell differentiation model was established to explore the role of the miR-3917/HLA-DRB1 axis in regulating CD4T cell differentiation into Th17 cells. STAT3 and RORγt levels were detected by RT-qPCR and WB. Production of IL-17 and IL-21 was determined by ELISA kits. MiR-3917 upregulation and HLA-DRB1 downregulation were detected in patients with CP. Overexpression of miR-3917 promoted the differentiation of CD4T cells toward Th17 cells, boosted the secretion of IL-17 and IL-21, and elevated the levels of STAT3 and RORγt, whereas inhibition of miR-3917 exerted the opposite effects. Rescue experiment confirmed that miR-3917 increased Th17 cell differentiation by directly targeting and regulating HLA-DRB1. MiR-3917 downregulated HLA-DRB1, thereby promoting Th17 cell differentiation and ultimately aggravating inflammation. These findings suggested that miR-3917 may be involved in CP pathogenesis and might serve as a potential diagnostic biomarker for CP. - Source: PubMed
Publication date: 2026/09/08
OuYang YuLuLi QiyanXie HuiminZhang TingtingDai Zhenhua - The functional status of regulatory T cells expressing the gut-homing receptor CCR9 (CCR9 Tregs) in type 1 diabetes mellitus (T1DM) remains unclear. This study aims to investigate the functional alterations of CCR9 Tregs in a T1DM model and evaluate the interventional effect of targeting the IL-21/IL-17 axis on their dysfunction. - Source: PubMed
Publication date: 2026/08/30
Xia YulianHe QingYao YuhuiYang LeiZhan ShanshanMao Shunfeng - HIV-1 reservoirs are predominantly located in CD4+ T-cells; however, not all CD4+ T-cells contribute to the reservoir in the same way. Factors such as activation, differentiation, and cell metabolism have been proposed to determine the relative susceptibility of cells to HIV-1 infection. HIV-1 reservoirs are seeded early during the acute phase of infection, but the cell composition of these reservoirs evolves in the transition to chronic infection. This suggests that there are factors during the acute phase that may alter the intrinsic susceptibility of CD4+ T-cells to HIV-1. We investigated here the influence of common cytokines known to be secreted during the acute phase and to play a role in either T cell homeostasis or HIV-1 infection on activation, differentiation, metabolic activity, and HIV-1 susceptibility of CD4+ T-cells. We show that the proinflammatory cytokines interleukin (IL)-2, IL-7, and IL-15 induce cellular activation, differentiation to effector profile, increase in metabolic capacity, and HIV-1 susceptibility. In contrast, IL-21, another cytokine from the gamma-chain (γc) family, showed opposing effects on the same parameters, including decreasing oxidative phosphorylation (OXPHOS) and HIV-1 infection. We also show that IL-10 and interferon (IFN)-α are able to at least partially revert the cellular and metabolic changes induced by IL-2 or IL-7 and reduce the cells' susceptibility to HIV-1. - Source: PubMed
Elfidha AmalDe la Torre Tarazona ErickPassaes CarolineAlcamí JoséMüller-Trutwin MichaelaSáez-Cirión Asier - In this work, we developed bispecific antibody (bsAb)-derived surrogate agonists which mimic the function of IL-21 by targeting the IL-21 receptor composed of IL-21 R (CD360) and IL-2 Rγ (CD132). For this, antigen-specific VHHs (variable domains of the heavy chain of heavy-chain-only antibodies) were obtained by immunization of camelids and isolated using yeast surface display. Combinatorial reformatting of IL-21 R-specific single‑domain antibodies (sdAbs) and IL-2 Rγ-targeting paratopes into a monovalent bispecific antibody architecture enabled the identification of IL-21 mimetics displaying attenuated capacities in triggering STAT3 phosphorylation compared to the wild-type cytokine as demonstrated in NK-92 cells as well as peripheral blood mononuclear cells (PBMCs). Moreover, by applying different protein engineering strategies, we demonstrate that agonism capacities of the generated IL-21 mimetics, such as pSTAT3 induction or Granzyme B expression of cytotoxic T cells, can be significantly optimized. For this, framework mutations were introduced to engineer VHH:VHH interactions within the bispecific sdAb-Fc fusion geometry for a more rigid receptor targeting. Furthermore, we show that antibody format engineering, in which the VHHs were arranged in an IgG-like scaffold that replaces the conventional IgG VH and VL domains with the corresponding VHHs, combined with rigidifying mutations, enables IL-21 R agonism comparable to the wild-type cytokine. Taken together, these findings show that IL-21 receptor agonism can be substantially optimized by adapting the spatial orientation of paratopes targeting both receptor subunits via forced dimerization, without altering paratope valencies. - Source: PubMed
Publication date: 2026/09/02
Lipinski BrittaUnmuth LauraTran Thi Hong HueHarwood JakobArras PaulBecker StefanHarwardt JuliaGuarnera EnricoHelming LauraZaynagetdinov RinatBertoldo DavideRajpal ArvindElter DesislavaPekar LukasEvers AndreasZielonka Stefan