IL21 polyclonal antibody (A01)
- Known as:
- IL21 pab (anti-) (A01)
- Catalog number:
- H00059067-A01
- Product Quantity:
- 50 uL
- Category:
- -
- Supplier:
- Abno
- Gene target:
- IL21 polyclonal antibody (A01)
Related genes to: IL21 polyclonal antibody (A01)
- Gene:
- ABRAXAS2 NIH gene
- Name:
- abraxas 2, BRISC complex subunit
- Previous symbol:
- KIAA0157, FAM175B
- Synonyms:
- Em:AC068896.4, ABRO1
- Chromosome:
- 10q26.13
- Locus Type:
- gene with protein product
- Date approved:
- 2004-03-16
- Date modifiied:
- 2017-04-27
- Gene:
- AKR1C3 NIH gene
- Name:
- aldo-keto reductase family 1 member C3
- Previous symbol:
- HSD17B5
- Synonyms:
- KIAA0119, DDX, HAKRB, PGFS
- Chromosome:
- 10p15.1
- Locus Type:
- gene with protein product
- Date approved:
- 1998-09-29
- Date modifiied:
- 2016-10-05
- Gene:
- ARHGAP4 NIH gene
- Name:
- Rho GTPase activating protein 4
- Previous symbol:
- -
- Synonyms:
- KIAA0131, C1, p115, RhoGAP4, SrGAP4
- Chromosome:
- Xq28
- Locus Type:
- gene with protein product
- Date approved:
- 1997-08-28
- Date modifiied:
- 2015-09-11
- Gene:
- ARHGEF7 NIH gene
- Name:
- Rho guanine nucleotide exchange factor 7
- Previous symbol:
- -
- Synonyms:
- KIAA0142, PIXB, DKFZp761K1021, Nbla10314, DKFZp686C12170, BETA-PIX, COOL1, P85SPR, P85, P85COOL1, P50BP, PAK3, P50
- Chromosome:
- 13q34
- Locus Type:
- gene with protein product
- Date approved:
- 2001-11-21
- Date modifiied:
- 2016-10-05
- Gene:
- BCLAF1 NIH gene
- Name:
- BCL2 associated transcription factor 1
- Previous symbol:
- -
- Synonyms:
- KIAA0164, BTF
- Chromosome:
- 6q23.3
- Locus Type:
- gene with protein product
- Date approved:
- 2004-01-13
- Date modifiied:
- 2017-06-09
Related products to: IL21 polyclonal antibody (A01)
Related articles to: IL21 polyclonal antibody (A01)
- Cancer-associated fibroblasts (CAFs) have been recognized as key contributors to tumor progression. Chimeric antigen receptor (CAR) T-cell therapy targeting fibroblast activation protein (FAP), a marker of CAFs, has gained attention and is being evaluated in both preclinical and clinical studies. Cord blood (CB)-derived CAR natural killer (NK) cell therapy has shown efficacy in hematologic malignancies. In this study, we generated FAP-targeting CAR NK cells (FAP-CAR NK cells). CD3-depleted CB mononuclear cells were stimulated with irradiated K562 cells expressing 4-1BB ligand (tumor necrosis factor ligand superfamily member 9) and membrane-bound interleukin-15 and interleukin-21 to expand NK cells, into which FAP-CAR was introduced. FAP-CAR NK cells produced cytokines and exerted cytotoxic activity when co-cultured with FAP-transduced HT1080 cells and CAFs isolated from human lung cancer tissue. In a xenograft model established by intrathoracic co-injection of A549 lung cancer cells and luciferase-expressing CAFs, injection of FAP-CAR NK cells, but not control CD19-CAR NK cells, resulted in their robust expansion and persistence in vivo for 5 weeks. However, CAFs were not eliminated by FAP-CAR NK cells, although CAR NK cells were clearly detected in the tumors. The levels of cytotoxicity-associated molecules (such as granzymes) were higher in FAP-CAR NK cells persisting in the spleens of mice compared with those in pre-infusion FAP-CAR NK cells. These results indicate that FAP-CAR NK cells have the potential to respond specifically to the target antigen and expand robustly in vivo, although further optimization is required to maintain cytotoxic function for a prolonged duration in vivo. - Source: PubMed
Publication date: 2026/09/20
Hiroshima TakashiKimura ToruMaekawa MarikoNoguchi MayukoMatsui TakahiroIkeda ShunyaSuga MakikoNagata HidekiKimura KenjiFukui ErikoKanou TakashiOse NaokoMorii EiichiShintani YasushiHosen Naoki - Cell-based immunotherapies of PBMC-derive Natural killer (NK) cells have demonstrated substantial potential for the treatment of hematologic malignancies. However, its application is limited due to the complex and inefficient gene modification and the insufficient therapeutic efficacy against solid tumors . - Source: PubMed
Publication date: 2026/09/03
Li YangyangWang YehaiZhang XimengFan YanPan LinaWu JingXiao Weihua - Spotty Liver Disease (SLD) is an acute bacterial infection of layer chickens in production, caused by Campylobacter hepaticus, and occurs most frequently in barn-housed and free-range systems. The disease is characterized by a sharp decline in egg production and increased mortality. The hallmark pathological feature is 1-2 mm white to grey necrotic foci distributed across the liver surface. Despite its growing economic impact on commercial poultry, the molecular mechanisms underlying host responses to C. hepaticus infection remain poorly understood. To address this gap, we performed a comprehensive transcriptome analysis of liver tissue from chickens naturally infected with SLD compared to uninfected controls. Illumina NovaSeq-based RNA sequencing was performed on liver tissues collected from three SLD-infected and three uninfected control chickens, with three biological samples for each sample type (n = 6), yielding 9,277 differentially expressed genes (DEGs), of which 3,063 were upregulated and 6,214 were downregulated. Functional pathway enrichment analysis revealed significant alterations in immune and metabolic processes associated with SLD pathophysiology. Infected chickens exhibited significant activation of immune response pathways, particularly cytokine-cytokine receptor interactions involving interleukins IL-22, IL-21, and IL-6, along with enhanced cell signaling, and cell adhesion. Among the individual genes, C1QTNF1 and the adhesion molecule gene ADGRD1 were notably overexpressed, indicating enhanced inflammatory activity. In contrast, core hepatic metabolic functions were profoundly reduced (adjusted p < 0.05) as evidenced by downregulation of oxidative phosphorylation, fatty acid metabolism, iron ion binding, and heme binding pathways. A marked increase in serum amyloid A (SAA) gene expression further indicated robust acute-phase responses and compromised liver function during infection. Together, these findings demonstrate a complex interplay between inflammatory activation and metabolic dysregulation during SLD. The strong upregulation of acute-phase proteins and pro-inflammatory cytokines demonstrates the host's vigorous attempt to combat bacterial infection, whereas the concurrent suppression of essential metabolic pathways reflects the pathological consequences of SLD. This study provides a transcriptomic characterization of host responses to C. hepaticus infection, offering insights into SLD pathogenesis and potential avenues for targeted intervention. - Source: PubMed
Publication date: 2026/09/16
Bommineni VarshaEdison Lekshmi KGottapu ChaitanyaButcher Gary DKariyawasam Subhashinie - Peri-implantitis is characterized by progressive tissue destruction accompanied by dysregulated innate and adaptive immune responses. This study evaluated whether systemic treatment with 2-deoxy-D-glucose (2-DG) could attenuate experimental peri-implantitis and alter inflammatory markers associated with macrophage- and T-cell-mediated responses in a rat model. Experimental peri-implantitis was induced in rats by Porphyromonas gingivalis-inoculated silk ligation around the implant neck. After disease induction, animals received intraperitoneal injections of 2-DG or normal saline for six weeks while ligature-associated challenge was maintained. Peri-implant tissues were assessed by micro-computed tomography (micro-CT), hematoxylin and eosin staining, immunohistochemistry (IHC), and reverse transcription-quantitative PCR (RT-qPCR). 2-DG treatment significantly reduced peri-implant bone resorption and was associated with less pronounced bone-resorptive morphology. RT-qPCR showed lower expression of M1-associated genes (, , , , and ) and the Th17-associated genes and , whereas , M2-associated genes, and the Treg-associated gene were not significantly changed. IHC showed qualitative trends toward lower iNOS- and IL-17-positive signals. These findings provide proof-of-concept evidence that 2-DG treatment reduces peri-implant bone loss and is associated with attenuated inflammatory changes and lower expression of M1- and Th17-associated inflammatory markers in experimental peri-implantitis. This study supports further investigation of 2-DG as a potential immunometabolic adjunct for peri-implantitis management. - Source: PubMed
Publication date: 2026/08/22
Deng ShudanLiu XingchenWu FeiyangChen ShouchengChen Zhuofan - Systemic lupus erythematosus (SLE) is a complex autoimmune disorder driven by aberrant immune responses, predominately CD4 + T cells dysfunction. CD73, an ecto-5'-nucleotidase mediating adenosine signalling, is essential for immune regulation. Herein, we investigated CD73 expression across CD4 + T subpopulations and further explored their potential impacts on the activation and function of CD4 + T subsets, together with their associations with disease activity and clinical features of SLE. A total of 134 SLE patients, 84 disease controls antiphospholipid syndrome (APS), and 61 healthy controls (HCs) were recruited. Flow cytometry was used to profile CD73 expression across circulating CD4 + T subsets. Disease activity was assessed by SLEDAI-2 K score. We identified a subset-specific distribution pattern of CD73 expression in SLE compared with HCs, characterized by increased CD73 expression in Th1 and Th17 cells and reduced expression in Th2, Tregs, Tfh and Tfr cells. Meanwhile, significant elevated CD73-expressing Th1/Th2 ratios and obviously reduced CD73-expressing Tfh/Tfr ratios in SLE were observed. CD73-expressing Th1 cells exhibited enhanced activation phenotype manifested as elevated expression of CD25, ICOS, PD-1, and secretion of IFN-γ. Positive correlation was observed between CD73-expressing Th1 cells and CD25 expression within Th1 cells. In addition, CD73-expressing Tph cells displayed reduced secretion of IFN-γ and IL-21, and positive association was found between CD73 expression and IL-21 secretion within Tph cells. Importantly, frequencies of CD73-expressing Th1, Th2 and Tph cells were significantly reduced in active disease group relative to inactive group, and negatively correlated with SLEDAI-2 K scores, and CD73-expressing Th1 cells displayed moderate discriminatory capacity (AUC = 0.671) to differentiate active and inactive SLE. Furthermore, SLE patients with lupus nephritis showed decreased CD73-expressing Th1 cells and Tph cells, and Tph cells was diminished in patients with thrombocytopenia. These findings highlighted CD73 as a potential marker of immune dysregulation, which may be associated with the activation- and function-related cellular phenotypes. Aberrant CD73 expression may potentially be associated with disease activity and clinical manifestations of SLE patients. - Source: PubMed
Publication date: 2026/09/13
Ma RuiYu Wen-JieYang Yun-XianLai Zhan-HongFeng Jing-HongLi Wen-YiLong Yan