Anti_human IL21R (ED) rabbit polyclonal
- Known as:
- Anti_human IL21R (ED) host: rabbit pab
- Catalog number:
- ASA905-308
- Product Quantity:
- 100 µg
- Category:
- -
- Supplier:
- Other suppliers
- Gene target:
- Anti_human IL21R () rabbit polyclonal
Related genes to: Anti_human IL21R (ED) rabbit polyclonal
- Gene:
- IL21R NIH gene
- Name:
- interleukin 21 receptor
- Previous symbol:
- -
- Synonyms:
- CD360
- Chromosome:
- 16p12.1
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-29
- Date modifiied:
- 2019-04-23
Related products to: Anti_human IL21R (ED) rabbit polyclonal
Related articles to: Anti_human IL21R (ED) rabbit polyclonal
- Severe combined immunodeficiency (SCID) comprises a group of life-threatening inborn errors of immunity (IEI) characterized by profound T-cell deficiency, frequently accompanied by impaired B cell and natural killer (NK) cell function. X-linked SCID (X-SCID), caused by pathogenic variants in , accounts for approximately 30% of all SCID cases. - Source: PubMed
Publication date: 2026/04/14
Gutiérrez-Zepeda Bricia MelissaLona-Reyes Juan CarlosCruz-Muñoz Mario ErnestoQuintero-Ramos AntonioTorres-Lozano CarlosBayardo-Gutierrez BeatrizBarrón-Balderas AlejandroRosenzweig Sergio DStoddard JenniferNiemela JulieNúñez-Núñez María Enriqueta - Cyprinid herpesvirus 3 (CyHV-3) is a pathogen that causes high mortality in common carp () and koi. Common carp breeding lines with different genetic backgrounds exhibit different resistance levels to viral pathogens. This study aimed to determine the differences in CyHV-3 disease resistance performance between the hybrid offspring (Y × M and M × Y) of the mirror carp 'Longke 11' (resistant to CyHV-3) and Yellow River carp, as well as the self-crossed offspring (M and Y). The M, Y × M, M × Y and Y groups were infected with CyHV-3 by immersion. The order of mortality and the duration of death for the four groups of carp were as follows: Y group > Y × M group > M × Y group > M group. Throughout the entire infection stage, the mRNA expression levels of the viral factors () and () in the four groups of carp tended to first increase but then decrease. The viral factor expression evaluated on days 30 and 31 post-infection (p.i.), which was the peak of infection mortality, was the highest in the Y group and the lowest in the M group, and compared with the Y × M group, the M × Y group had considerably lower viral gene expression ( < 0.05). The immune-related enzyme activity and content levels of the four carp groups matched the patterns of viral gene expression. On day 29 p.i., a time point with high mortality, the levels of alkaline phosphatase (AKP), glutathione peroxidase (GSH-Px) and total antioxidant capacity (T-AOC) were significantly the lowest in the Y group and significantly the highest in the M group, while the Y × M group showed a significant decrease compared to the M × Y group ( < 0.05). Quantitative real-time (q-PCR) analysis revealed that (), (), (), interleukin-6 () and (), exhibited an initial increase followed by a decrease among the four experimental groups of common carp. In the peak mortality period of carp in the four groups (30 days post-infection), the expression levels of , , , and were significantly the highest in the M group and significantly the lowest in the Y group, with the mRNA expression of these genes in the M × Y group being significantly higher than that in the Y × M group ( < 0.05). In contrast, expression levels exhibited the opposite trend. In this study, the M group exhibited the greatest resistance to CyHV-3, followed by the M × Y group, whose resistance was greater than that of the Y × M group, with the Y group showing the lowest disease resistance. Our findings demonstrate that hybridization modulates resistance to CyHV-3. Furthermore, we identified conserved immune signatures common to both susceptible and resistant carp, including the activation of nonspecific immunity and the upregulation of immune-associated genes. - Source: PubMed
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Jiang XiaonaSong ZhenguoLi ChitaoHu XuesongGe YanlongCheng LeiShi XiaodanDi YaxinJia Zhiying - Interleukin-15 (IL-15) has emerged as a central cytokine for next-generation cancer immunotherapy because of its unique ability to sustain the survival, proliferation, and cytotoxic function of memory CD8 T cells and natural killer (NK) cells without promoting the expansion of regulatory T cells (Treg). These properties make IL-15 particularly attractive for achieving durable antitumor immunity, especially in solid tumors where immune persistence remains a major limitation. Although IL-15 shares the same signal-transducing receptor subunits (IL-2R and the common chain) with interleukin-2 (IL-2), the two cytokines drive fundamentally different CD8 T-cell fates, a distinction that underlies their markedly divergent therapeutic profiles in cancer immunotherapy. In recent years, multiple IL-15-based therapeutic strategies including recombinant IL-15, and IL-15 immunocytokines have entered clinical evaluation, demonstrating potent immune activation with manageable toxicity profiles. Recent clinical progress includes the FDA approval of Nogapendekin alfa inbakicept (N-803), the first IL-15-based immunotherapy approved for cancer treatment, alongside the advancement of other IL-15 superagonists into Phase II trials and growing evidence that IL-15 can enhance the efficacy of immune checkpoint blockade and engineered adoptive cell therapies such as CAR-T cells, CAR-NK cells, T cells, and invariant NKT cells. Despite these advances, important challenges remain, including cytokine-associated toxicities, optimal delivery strategies, and the immunosuppressive tumor microenvironment. This review summarizes recent progress in IL-15-based cancer immunotherapy, integrates emerging insights into IL-2R-driven CD8 T-cell fate decisions, and discusses key opportunities and challenges for translating IL-15-mediated immune enhancement into durable clinical benefit. - Source: PubMed
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Gao HuiquanMa TaoJiang QinqinGao LanfangLi JinfangWang ShuboLiu ZiyongZhang ZhixinWu GangHe WenxinZhou Fuxin - Interleukin-2 receptor γ chain (IL2RG, CD132) act as a signaling subunits for various cytokine receptors, required for lymphocyte growth and maturation. Genetic variants within the IL2RG gene are associated with X-linked Severe Combined Immunodeficiency (X-SCID) disease. This study uses an method to investigate the structural and functional impacts of two IL2RG variants, Trp240Arg (W240R) and Arg226Cys (R226C), located in the extracellular domain, a region important for receptor stability. Homology modeling was generated for Wild-Type (WT) and Variant IL2RG structures and subsequently analyzed through Molecular Dynamics (MD) simulations and protein-protein docking utilizing IL-2 and IL-21 cytokines. MD simulations showed that WT-IL2RG remained stable, whereas its variant exhibited structural instability. W240R is disrupted by increased solvent exposure and reduced compactness. The IL-2 binding caused structural alterations in the WT complex in cytokine-bound states, whereas R226C reduced hydrogen bonds to decrease binding, and W240R increased flexibility to destabilize the interface. The WT complex exhibited consistent hydrogen bonding and was the most stable for IL-21, whereas both variants displayed weaker interactions and fluctuations. Further, the binding free energy Molecular Mechanics-Poisson Boltzmann Surface Area (MM/PBSA) analysis confirmed that WT complexes had better binding (IL-2: -40.87 kJ/mol; IL-21: -45.88 kcal/mol) compared to R226C (-35.42, -34.67 kcal/mol) and W240R (-29.54, -33.30 kcal/mol). The study reveals that Trp240Arg and Arg226Cys variants in IL2RG negatively affect cytokine-receptor interactions, lower binding energetics, and disturb the structural integrity of IL2RG, shedding light on the mechanisms underlying IL2RG-associated immunodeficiency disorders. - Source: PubMed
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S AswiniS Asha Devi - Aberrant differentiation of T follicular helper (Tfh) cells contributes to the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE). However, whether Tfh cell differentiation is regulated by glycosylation remains unclear. In this study, we found that inhibition of N-glycosylation completely blocked Tfh cell differentiation. Critical molecules that define Tfh cell function, including CXCR5, PD-1, and IL-21, were found to contain multiple N-glycosylation motifs (conserved Asn-X-Ser/Thr sequences) based on amino acid sequence analysis. Notably, multiple genes encoding enzymes involved in different stages of N-glycosylation were highly expressed in peripheral CD4 T cells from patients with SLE, particularly in those with active disease. Together, these findings implicate the role of N-glycosylation in the regulation of aberrant Tfh cell differentiation. Further elucidation of the mechanisms underlying N-glycosylation dysregulation in SLE will provide a critical foundation for understanding disease pathogenesis and facilitating the identification of novel therapeutic targets. - Source: PubMed
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