Interleukin_21 _ IL21
- Known as:
- Interleukin_21 _ IL21
- Catalog number:
- GTX18495
- 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
- Systemic lupus erythematosus (SLE) is a multi-organ autoimmune disease. B cells play a crucial role in disease initiation and progression. Clinical trial evidence suggests that intensified B-cell depletion can improve SLE therapeutic outcomes. While efficacy and tolerability of belimumab, the first B-cell-targeted agent approved for SLE, have been demonstrated, around 30-40% of patients still show suboptimal treatment response. Interleukin-21 (IL-21), a regulator of B-cell development, is closely associated with disease activity in SLE, underscoring its potential as a therapeutic target. However, monotherapy targeting IL-21 has yielded limited efficacy in clinical trials. - Source: PubMed
Publication date: 2026/08/27
Feng XiweiLong DiYin HuiqiLi LimingWang ZijunZhao JunpengFan XinyuWu WeiWu HaijingLu Qianjin - Osteoporosis (OP) is a chronic metabolic bone disease characterized by reduced bone mass, microarchitectural deterioration, and an increased risk of fragility fractures. Although conventional views have emphasized the imbalance between osteoblasts and osteoclasts, advances in osteoimmunology have shown that T-cell subsets regulate bone remodeling through multilayered mechanisms, including the RANKL/RANK/OPG axis, inflammatory cytokine networks, costimulatory molecules, immune checkpoints, the gut microbiota, and cellular metabolic reprogramming. Th17 cells and their signature cytokine IL-17 promote RANKL expression and amplify the NF-κB/MAPK/NFATc1 pathway of osteoclast differentiation, thereby constituting a key pathogenic component in inflammatory bone loss and postmenopausal osteoporosis. In contrast, regulatory T cells (Tregs) inhibit osteoclast formation through Foxp3-, IL-10-, TGF-β-, CTLA-4- and IDO-related pathways, thereby limiting proinflammatory T-cell activation and maintaining bone marrow immune homeostasis. Th1/Th2 cells, CD8+ T cells, γδ T cells, T follicular helper cells, NKT cells, and mucosa-associated unconventional T cells may also influence bone resorption and formation in different pathological contexts through factors such as IFN-γ, TNF-α, IL-4, IL-13, IL-21, IL-22, and membrane-bound RANKL. Drawing on the literature concerning T-cell subsets, the Th17/Tregs and Th1/Th2 balances, γδ T cells, and the RANKL/OPG axis, this review provides a narrative synthesis of current evidence about the molecular mechanisms by which T-cell subsets regulate osteoporosis-related bone remodeling, the features of immune imbalance in different types of osteoporosis, T-cell-targeted intervention strategies, and translational challenges. The aim is to provide a theoretical basis for developing precision antiosteoporotic therapies from an osteoimmune perspective. - Source: PubMed
Publication date: 2026/08/11
Gong YuanZeng WenxingLiao YitaoXie XuanyuQin ZhichaoLi ChaoZhang Xian - Photodynamic priming (PDP), a fallout of photodynamic therapy, transiently modulates the tumor microenvironment (TME), enhances therapeutic susceptibility, and promotes immunogenic cell death through the release of damage-associated molecular patterns (DAMPs). Pancreatic ductal adenocarcinoma (PDAC) remains non-responsive to current therapies with a desmoplastic and immunosuppressive TME that limits drug delivery and blunts responses to immune checkpoint blockade. We investigated whether PDP could enhance anti-PD1 therapy responses in PDAC using patient-derived organoids (PDOs). PDOs were treated with Visudyne and red light (25, 75, and 100 J/cm²), followed by assessment of cytotoxicity, DAMP expression (HSP60, calreticulin, HMGB1), and transcriptomic changes. Monocyte-derived dendritic cells (mDCs) from healthy donors were cocultured with PDP-treated (25 J/cm) PDOs, then with matched naïve T cells. mDC and T cell activation markers were analyzed. Pembrolizumab (anti-PD1) was added to PDO-mDC-T cell cocultures to evaluate combined effects on PDO viability and T cell activation. PDP induced dose-dependent cytotoxicity and upregulated DAMPs. Gene profiling in PDOs showed increased , , and , with reduced , , and expression. mDCs exposed to PDP-treated PDOs upregulated CD40, CD86, and MHC-II, driving activation of CD4 and CD8 T cells, evidenced by elevated PD1 expression. Addition of pembrolizumab further decreased PDO viability and amplified effector cytokines (, , , B, , ). PDP was associated with modulation of the PDAC TME toward a more immunogenic phenotype by enhancing tumor immunogenicity, activating dendritic cells and T cells, and potentiating PD1 blockade. These findings provide mechanistic support for further preclinical and clinical evaluation of PDP combined with checkpoint inhibition in PDAC. - Source: PubMed
Publication date: 2026/08/11
De Silva PushpamaliWekking DemiChoe Joanna JoeunKidd Madeline DPearce Josie LRocha Castellanos Dario MissaelZelga PiotrJenkins RussellWang Kenneth KChandrasekhara VinayMaytin Edward VLiss Andrew ScottHasan Tayyaba - Age-associated B cells (ABCs) are a dynamic B cell subset whose identity, development, and function are fundamentally shaped by the tissue microenvironments in which they reside. Primarily defined by expression of CD11c and T-bet, ABCs arise across diverse contexts, including aging, infection, autoimmunity, and cancer, yet exhibit striking heterogeneity that reflects the distinct signals present in each tissue niche. While the core generative cues of TLR7/9 activation, IFN-γ, IL-21, and BCR stimulation are common, the local tissue environment dictates how these signals are integrated and which functional properties are ultimately expressed. In infectious environments, altered splenic structure, peripheral tissue inflammation, and organ-specific cytokine gradients influence context-dependent ABC phenotypes with unique localization and effector characteristics. In autoimmune diseases, target organ microenvironments provide the TLR ligands, cytokines, and cellular interactions that sustain local ABC expansion and pathogenic activity. Similarly, in the tumor microenvironment, ABCs are shaped by tertiary lymphoid structures and chronic inflammatory signals that can shift their function between pro-inflammatory and immunosuppressive states. This review explores how tissue microenvironments influence ABC biology in infections, autoimmunity, and cancer, highlighting critical implications for understanding disease mechanisms and developing targeted therapeutic strategies. - Source: PubMed
Francis Rebecca LWeinstein Jason S - To investigate the role of lipopolysaccharide (LPS)-mediated toll-like receptor 4 (TLR4) signaling in modulating the tumor immune microenvironment, particularly the follicular helper T cell (Tfh)/follicular regulatory T cell (Tfr) equilibrium, in bladder cancer. - Source: PubMed
Publication date: 2026/07/15
Peng BoWang YanLi HaochenZhuang ChangshuiGuan RijianZhang HaopengWan Lijun