Human IL21 protein Proteins
- Known as:
- Human IL21 protein Proteins
- Catalog number:
- orb82725
- Product Quantity:
- 1 mg
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Human IL21 protein Proteins
Related genes to: Human IL21 protein Proteins
- 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: Human IL21 protein Proteins
Related articles to: Human IL21 protein Proteins
- Hepatocellular carcinoma (HCC) remains a significant global health threat characterized by aggressive progression and high mortality rates. Despite therapeutic advancements, survival for advanced stages is unacceptably low, necessitating innovative approaches like Natural Killer (NK) cell-based immunotherapy. NK cells are crucial innate immune components providing rapid tumor cytotoxicity without prior sensitization. However, the HCC tumor microenvironment (TME) presents a formidable barrier, inducing NK cell dysfunction through immunosuppressive cytokines like TGF-[Formula: see text], chronic hypoxia, and metabolic exhaustion driven by lipid accumulation. This literature review consolidates and integrates findings regarding current NK cell-based strategies in HCC, with particular emphasis on mechanisms of NK cell dysfunction within the TME and therapeutic approaches designed to restore their antitumor activity. Emerging therapeutic strategies involve cytokine-supported approaches, including the adoptive transfer of autologous or allogeneic NK cells expanded ex vivo using stimuli such as IL-15 and IL-21. In parallel, advances in genetic engineering have enabled the development of modified NK cells, including chimeric antigen receptor (CAR)-NK platforms targeting HCC-associated antigens such as glypican-3 (GPC3) and CD147 and bispecific and trispecific killer cell engagers (BiKEs and TriKEs). This review underscores the translational potential of NK cell-based therapies by highlighting unresolved knowledge gaps in the complex interplay between NK cells and the TME. These developments provide a foundation for optimizing NK cell immunotherapy and improving prognostic outcomes for patients with HCC. - Source: PubMed
Publication date: 2026/09/24
Widowati WahyuWargasetia Teresa LilianaSadri BaharehNainggolan Ita MargarethaAzis RizalRifana Safira DindaRismani ElhamVosough Massoud - Precision-cut lymph node slices (PCLNS) provide a physiologically relevant ex vivo model to investigate lymphoid immune activation and vaccine adjuvant function while preserving native tissue architecture. In this study, we established for the first time porcine PCLNS and assessed the immunostimulatory capacity of PCLNS to Toll-like receptor (TLR) 7/8 agonist (Resiquimod; R848) alone or in combination with porcine circovirus type 2 (PCV2) or PCV2 virus-like particles (VLPs). - Source: PubMed
Publication date: 2026/09/09
Deosthali SamruddhiMarti-Garcia BernatHarris HeatherWerling NatalieNoad RobertGerner WilhelmWerling Dirk - Pancreatic ductal adenocarcinoma (PDAC) is refractory to most therapies, including immunotherapies, for which reinvigoration of CD8 T cells through immune checkpoint blockade is insufficient to induce long-term, durable remissions. Direct KRAS inhibitors (KRASi) have shown clinical promise, although acquired resistance is common. We modeled KRASi response and relapse in mice and demonstrated that, unlike chemotherapy or combinations with checkpoint blockade, an interleukin (IL)-21 cytokine mimic (21h10) induced long-term, durable remissions. Its efficacy depends on T helper 1 (Th1)-polarized CD4 T cells, but not on CD8 T cells or tumor cell expression of major histocompatibility complex class I (MHC class I). Specifically, CD4 T cells primed by type 2 conventional dendritic cells (cDC2s) produce interferon γ (IFN-γ), which promotes macrophage-mediated phagocytosis of tumor cells. Ex vivo treatment of human PDAC specimens with 21h10 induces IFN-γ production by infiltrating T cells. Thus, IL-21-elicited CD4 T cells exert antitumor activity in mice and potentially in humans, converting transient responses to KRAS inhibition into durable remissions. - Source: PubMed
Publication date: 2026/09/23
Qiang LiHoffman Megan TChun Jung-HoParent BrendanHambitzer FelixPeprah FrankKureshi Courtney T SLim Birkley SChang EugenaWalsh Michael JTello Julissa GAtajanova TavusShin HojeongPerkins CoreyKureshi RakeebMolina-Aponte YanirisDougan James MZuo ChongBrais LaurenClancy Thomas ECleary James MHornick Jason LHuffman Brandon MMancias Joseph DMolina GeorgeFairweather MarkNowak Jonathan APerez Kimberly JRubinson Douglas ASlater Sarahvan Dams RitchellWang JipingWolpin Brian MWong Kwok-KinSingh HarshabadAguirre Andrew JBaker DavidDougan MichaelDougan Stephanie K - Aging is a major risk factor for atherosclerosis and is accompanied by profound changes in the immune system, including effector T cell expansion, senescent cell accumulation, and increased pro-inflammatory signaling. Rapamycin, a promising rejuvenation therapeutic that inhibits mTORC1 and modulates immune aging, was investigated for its potential to attenuate pro-atherogenic immune responses in aged atherosclerotic mice. 80- to 90-week-old male Ldlr mice with established atherosclerotic lesions were treated intraperitoneally with rapamycin or control triweekly for 8 weeks. Systemic and plaque immunity was assessed by flow cytometry or single-cell RNA-sequencing. Plaque morphology was evaluated by histology. Rapamycin treatment reduced plaque macrophage content (0.73 ± 0.07 × 10 μm) compared to control (ctrl: 0.95 ± 0.09 × 10 μm, p < 0.05) and decreased total T cell numbers in vascular and lymphoid tissues. This was accompanied by a shift from effector to central memory phenotypes, particularly within the CD8 compartment, and a relative enrichment of regulatory CD4 T cells (Tregs). Single-cell transcriptomics of aortic Tregs revealed increased expression of suppressive genes (Foxp3, Tgfb1) upon rapamycin. Rapamycin also reduced T follicular helper cells, IL-21 expression, germinal center B cells, plasma cells, and total and oxidation-specific epitope-specific immunoglobulin levels. Additionally, age-associated B cells were diminished in spleen and lymph nodes, reflecting a broader anti-inflammatory effect on B cell immunity. Finally, aortic leukocytes displayed profoundly reduced senescent enrichment scores. Rapamycin remodels the immune landscape in aged atherosclerotic mice, promoting regulatory lymphocyte subsets and suppressing antigen-driven and inflammatory immune responses. These findings highlight the potential of immune-targeted rejuvenation to mitigate age-related atherogenic inflammation. - Source: PubMed
de Mol Jillde Korte Daphne HDepuydt Marie A CSmit VirginiaKleijn Mireia N A Bernabévan Santbrink Peter JBinder Christoph JPorsch FlorentinaSchaftenaar Frank HFoks Amanda C - 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