IL21 - Rabbit polyclonal to IL21 Polyclonal
- Known as:
- IL21 - Rabbit pab IL21 Polyclonal
- Catalog number:
- 18-272-196680
- Product Quantity:
- 0.05 mg
- Category:
- -
- Supplier:
- GenWay
- Gene target:
- IL21 - Rabbit polyclonal Polyclonal
Related genes to: IL21 - Rabbit polyclonal to IL21 Polyclonal
- 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
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guanine nucleotide binding protein alpha inhibiting activity polypeptide 1 (GNAI1) polyclonal antibody kinase suppressor of ras (KSR) polyclonal antibody(Alpha)_ 1 _ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_ Feto Protein (AFP) POLYCLONAL Rabbit anti_human(Alpha)_1_ antitrypsin (A1AT) POLYCLONAL Rabbit anti_human(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,b_cyclohexyl_Ala8,D_Tic16,Arg17,Cys18)_Atrial Natriuretic Factor (6_18) amide (mouse, rabbit, rat) Salt _ Binding (Disulfide_bond) Synonym A71915 SumFormula C69H116N26O15S2(Arg6,β-cyclohexyl-Ala8,D-Tic16,Arg17,Cys18)-Atrial Natriuretic Factor (6-18) amide (mouse, rabbit, rat)
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- Common variable immunodeficiency (CVID) is frequently complicated by autoimmune and inflammatory manifestations associated with profound immune dysregulation (CVIDc), including expansion of T-betCD21 B cells (CD21 B cells). Elevated serum IL-10 levels have repeatedly been reported in CVIDc, yet their relationship to CD21 B-cell differentiation remains unclear. In this study, we determined a significant correlation between increased serum IL-10 levels and frequency of circulating CD21 B cells, particularly marked in CVIDc patients. Transcriptomic and protein analyses identified multiple cellular sources of IL-10 in CVID, including monocytes, T cells, and a subset of CD21 B cells in peripheral blood and inflamed tissues. CD21 B cells expressed elevated levels of IL-10 receptor subunits and displayed intact IL-10-induced STAT3 signaling, indicating preserved responsiveness to IL-10. Functionally, IL-10 alone neither induced CD21 B-cell differentiation nor inhibited IFN-γ-driven polarization. However, in vitro differentiation assays showed that IL-10 can substitute for IL-21 during CD40L/T cell-dependent differentiation of CD21-like B cells and promote their survival in vitro. These findings suggest that IL-10 may support the expansion and persistence of CD21 B cells at inflammatory sites. Collectively, our data identify IL-10 as a component of the inflammatory environment associated with CD21 B-cell expansion and suggest that IL-10 can functionally replace IL-21 during their differentiation and promote their survival in CVID-associated immune dysregulation. - Source: PubMed
Publication date: 2026/08/15
Cousin VictoriaGraumann AnnaGeiger ValerieSökler DavidBez PatrickGutenberger SylviaGlaser CorneliaAndrieux GeoffroyBoerries MelanieFrye Björn ChristianZissel GernotCalvillo Celia LourdesRodriguez-Ubreva JavierBallestar EstebanHauck FabianVoll Reinhard EChevalier NinaKeller BaerbelWarnatz Klaus - Anti-interferon-γ (IFN-γ) autoantibody (AAb)-associated adult-onset immunodeficiency (AOID) is an emerging disorder in East Asian adults characterized by severe opportunistic infections despite negative HIV status. The mechanisms driving anti-IFN-γ AAb production remain unclear. This study investigated B-cell gene expression, serum cytokine profiles, associations with AAb levels, and IFN-γ genetic variations in AOID patients. A cross-sectional study was conducted in 63 AOID patients and 30 healthy controls at Chiang Mai University Hospital, Thailand. Patients were classified as active or inactive according to infection status. B-cell gene expression, serum cytokines, anti-IFN-γ Aabs levels, and IFN-γ polymorphisms were analyzed by quantitative PCR, multiplex assays, ELISA, and nucleotide sequencing, respectively. AOID patients exhibited increased and expression and reduced , , , and expression. Active patients had higher levels of TNF-α, IL-6, IL-17A, IL-10, IL-21, and more chemokines than inactive patients. AAb levels positively correlated with TNF-α, IL-6, and IL-10. Correlation analysis showed positive associations among , , and , and a negative association between and . No significant IFN-γ sequence differences were identified within the analyzed transcript region. These findings suggest altered B-cell gene expression and inflammatory cytokine profiles in AOID, which may be associated with the immunological alterations observed in these patients and may provide insights into potential mechanisms underlying anti-IFN-γ AAb production. - Source: PubMed
Publication date: 2026/08/04
Rattanathammethee KritsadeeChawansuntati KriangkraiLumjuan NongkranNusartsang NattayaChaiwarith RomaneePraparattanapan JutaratSupparatpinyo KhuanchaiWipasa Jiraprapa - Chimeric antigen receptor (CAR)-T therapy has achieved partial therapeutic efficacy in solid tumors, but its overall effectiveness remains limited. IL-21-armored CD276.CAR-T (IL21.CD276.CAR-T) represents a promising strategy to enhance anti-tumor activity against esophageal squamous cell carcinoma (ESCC). However, resistance mechanisms remain unclear. We generated IL21.CD276.CAR-T cells and evaluated their cytotoxicity and in B-NDG xenograft models. Poliovirus receptor (PVR) expression on ESCC cells was analyzed, and shRNA-mediated knockdown was performed to validate its role in resistance. IL-21R expression on ESCC cells was examined to exclude direct IL-21 signaling. IL-21 enhances the cytotoxicity of CD276.CAR-T cells against ESCC. Although IL21.CD276.CAR-T exhibited potent cytotoxicity , it failed to achieve complete tumor regression, and resistant cells still emerged. Mechanistically, resistance was not caused by CD276 antigen loss or IL-21R expression, but by upregulation of PVR on cancer cell membrane after IL21.CAR-T exposure. knockdown restored CAR-T sensitivity , enhanced the anti-tumor capacity of IL21.CD276.CAR-T cells, and partially improved anti-tumor efficacy without systemic toxicity. PVR may act as a mediator of resistance to IL21.CD276.CAR-T in ESCC. Targeting PVR represents a novel strategy to overcome IL21.CAR-T resistance and improve therapeutic outcomes in ESCC. - Source: PubMed
Publication date: 2026/07/28
Wang LihongGuo QijingHan WenkaiTao XiaoxuanYe TongSun LiGao YimingNiu AnnaZhao HuiLiu XiaoyanWang Yu - γδ intraepithelial lymphocytes (IELs) are persistently expanded in the intestinal epithelium of patients with active celiac disease (ACeD), but their functional profile during active inflammation remains poorly defined. This study investigated the expression of pro- and anti-inflammatory cytokines in γδ IELs isolated from the intestinal epithelium of ACeD patients at different stages of mucosal damage. Frozen jejunum sections were obtained from 14 ACeD patients (7 Marsh II and 7 Marsh III) and 10 treated celiac disease (CeD) patients. γδ IELs from ACeD biopsies and intestinal enterocytes (IEs) from treated CeD biopsies were isolated by laser capture microdissection on mirror sections, followed by RNA extraction and quantitative real-time RT-PCR analysis of IL-15, IL-17A, IL-21, IFN-γ, TNF-α, IL-10, and TGF-β. Foxp3 expression was assessed by immunohistochemistry. γδ IELs from Marsh III biopsies showed significantly increased mRNA levels of IL-15, IL-17A, IL-21, IFN-γ, and TGF-β compared with IEs, whereas IL-10 expression was significantly higher in Marsh II γδ IELs compared with Marsh III and IEs. IL-21 and TGF-β were also higher in Marsh III than Marsh II γδ IELs. All γδ IELs were Foxp3. These findings indicate a stage-dependent functional polarization of γδ IELs in ACeD, with an IL-10-associated regulatory profile in Marsh II and a predominant pro-inflammatory cytokine signature in Marsh III. - Source: PubMed
Publication date: 2026/08/06
Mazzarella GiuseppeIacomino GiuseppeIaquinto GaetanoCamarca AlessandraPicariello ErricoMelina RaffaeleRotondi Aufiero Vera - To investigate the therapeutic mechanism of Formula (SJF) for alleviating rheumatoid arthritis (RA) with wind-cold-dampness arthralgia syndrome (WCDA) from the perspective of Th17/Treg immune balance. - Source: PubMed
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