Interleukin_21 _ IL21
- Known as:
- Interleukin_21 _ IL21
- Catalog number:
- AP09162PU-N
- Product Quantity:
- 0.1 mg
- 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
- 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 - Despite advancements in modern medicine, tuberculosis continues to be one of the leading causes of death globally. Findings indicate that COVID-19 may trigger the activation of tuberculosis infection (TB), leading to its spread. Despite the development of new immunological diagnostic methods for latent tuberculosis infection (LTBI), it is still unclear how the infection transitions to an active TB state. The goal of the study is to provide insights into the progression of tuberculosis infection from a latent to an active state. This article presents recent research data focused on investigating the pathogenesis of LTBI, particularly the immune responses in the interaction between (Mtb) and the host. It describes the mechanisms of T-cell immunity and cytokine activation, supporting the concept of type 1, type 2, and type 3 immune responses. According to the conducted studies, Th17 cells have a significant role in the development of type 3 antigen-specific responses. The cytokines IL-6 and IL-23 activate STAT3, which is necessary to trigger the expression of Th17. Future research on the role of Th17 cells and cytokines, particularly IL-6 and IL-21, may be beneficial in understanding the shift from LTBI to active TB. - Source: PubMed
Publication date: 2024/09/30
Kudryavtsev IgorStarshinova AnnaRubinstein ArtemKulpina AnastasiaLing HongZhuang MinKudlay Dmitry - Our objective was to conduct a review of host blood-derived biomarkers as potential diagnostic targets for pulmonary TB and as alternative tests to identify active tuberculosis in HIV co-infected individuals. - Source: PubMed
Publication date: 2025/01/08
Rapulana Antony MMpotje ThaboMthiyane NondumisoSmit Theresa KMcHugh Timothy DMarakalala Mohlopheni J - 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 - Personalized neoantigen (neoAg) vaccines have shown clinical promise in solid tumors , yet their efficacy and mechanism of action in hematopoietic malignancies remain poorly defined . Herein, we establish an immunocompetent syngeneic A20 B-cell lymphoma platform to test the efficacy of neoAg vaccines used either as mono- or combinatorial therapies with other immunotherapies . Whereas subcutaneous A20 tumors were refractory to single-agent αPD-1 or αCTLA4 therapy, they were eradicated in a T cell-dependent manner in 90% of syngeneic hosts treated with dual immune checkpoint therapy (dual ICT, i.e., αPD-1 + αCTLA4). By mapping antigen specificity of dual-ICT-elicited T cells, we identified and validated dominant endogenous A20 MHC-I and MHC-II neoantigens and designed therapeutic synthetic long peptide (SLP) vaccines containing these neoepitopes. This vaccine (A20 neoVAX) promoted robust neoAg-specific CD4□ and CD8□ T cell responses in naïve syngeneic BALB/c mice and induced tumor rejection in ∼70% of subcutaneous tumor-bearing mice. In addition, nearly all mice rejected their subcutaneous A20 tumors when A20 neoVAX was combined with αPD-1. To render the results of this study more physiologic, we developed a systemic A20 lymphoma model and found that dual ICT failed to control tumor progression and A20 neoVAX delayed tumor progression and prolonged animal survival but did not induce tumor rejection. In contrast, A20 neoVAX plus dual ICT achieved durable systemic tumor elimination. Mechanistically, the combination of A20 neoVAX plus dual ICT amplified priming of A20 neoAg-specific T cells, prevented T cell dysfunction, sustained the cytotoxic capacity of tumor-specific CD8 T cells, and induced Th1-skewing of CD4 T cells in tumor and peripheral compartments. To increase the clinical relevance of these findings and to minimize potential adverse events in tumor-bearing, therapeutically treated individuals, we substituted CD8-targeted cytokine muteins (CD8-IL2 or CD8-IL21) for αCTLA4. These agents represent genetically modified forms of IL-2 or IL-21 that selectively stimulate CD8 T cells but have significantly reduced capacity to activate chronic inflammation and immunosuppressive functions of other immune cells. Whereas mice bearing systemic A20 lymphoma treated with either nothing, A20 neoVAX, or A20 neoVAX + CD8-IL2 failed to control tumor outgrowth, 66.7% of tumor-bearing mice treated with A20 neoVAX + CD8-IL2 + αPD-1 rejected their tumors. In similar experiments in which CD8-IL21 was substituted for CD8-IL2, tumor clearance was also observed in two-thirds of A20-bearing mice but now rejection occurred in the absence of αPD1. Together, these data define a framework for optimal personalized neoAg vaccination in B-lymphoma and demonstrate that neoAg vaccines can safely synergize with CD8 T cell-selective immunotherapies to prevent T-cell dysfunction and generate durable systemic anti-tumor immunity. - Source: PubMed
Publication date: 2026/08/06
Song YuangAladyeva EkaterinaVieira Medrano Ruan FTheisen Derek JArthur Cora DWhite J MichaelKohlmiller Heather BrinkVomund AnthonySinghal KartikHoang MyAmeh SamuelSheehan Kathleen C FLevy RonaldFehniger Todd AArtyomov Maxim NGriffith MalachiGriffith Obi LYeung Yik AndyDjuretic IvanaSultan HusseinSchreiber Robert D