Rat IL21 protein Proteins
- Known as:
- Rat IL21 protein Proteins
- Catalog number:
- orb82622
- Product Quantity:
- 2
- Category:
- -
- Supplier:
- Biorb
- Gene target:
- Rat IL21 protein Proteins
Related genes to: Rat IL21 protein Proteins
- 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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- 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 - Psoriasis is a chronic inflammatory skin disorder characterized by dysregulated cytokine signaling and keratinocyte hyperproliferation, in which extracellular vesicles, particularly exosomes, play key roles in mediating intercellular inflammatory communication. In this study, we evaluated the pharmacological effects of calpeptin and bisindolylmaleimide I (BIM-I), inhibitors of calpain and protein kinase C previously reported to modulate extracellular vesicle-associated pathways, in a 3-dimensional human psoriatic skin model. Both inhibitors significantly reduced the expression of proinflammatory cytokines, keratinocyte activation marker, and exosome-related marker, including interleukin (IL)-1β, tumor necrosis factor-α, IL-8, interferon gamma, IL-21, IL-20, CC chemokine ligand-20, keratin 6A, CD9, and CD63, consistent with attenuation of psoriasis-associated inflammatory signaling. BIM-I additionally suppressed IL-22 and IL-6 expression and restored epidermal ultrastructural features, including desmosome density, to levels comparable with normal skin. Integrated proteomic and immunohistochemical analyses revealed distinct downstream biological responses associated with modulation of exosome-associated markers and pathways. Calpeptin treatment was associated with enrichment of endoplasmic reticulum stress-related pathways, as indicated by increased growth arrest and DNA damage-inducible protein 153 and glucose-regulated protein 78 expression, whereas BIM-I preferentially regulated cytoskeletal organization and keratinocyte differentiation, accompanied by reduced expression of growth arrest and DNA damage-inducible protein 153, glucose-regulated protein 78, and keratin 16. Collectively, these findings demonstrate that pharmacological inhibition of calpain and protein kinase C attenuates psoriatic inflammation and epidermal dysregulation and is associated with modulation of exosome-associated markers and pathways, together with differential regulation of endoplasmic reticulum stress and cytoskeletal networks. SIGNIFICANCE STATEMENT: This study demonstrates that pharmacological inhibition of calpain and protein kinase C attenuates inflammatory signaling and keratinocyte activation in a 3-dimensional psoriatic skin model, highlighting exosome-associated pathways as key regulators of disease pathology. Distinct mechanisms involving endoplasmic reticulum stress modulation and cytoskeletal regulation provide insight into how targeting vesicle-mediated intercellular communication may offer therapeutic potential in psoriasis. - Source: PubMed
Publication date: 2026/08/25
Fongsodsri KamonpanSomkaew WasaratAramwit PornanongReamtong OnrapakThiangtrongjit TipparatKanjanapruthipong TapaneeMuangkaew WatcharamatSukphopetch PassaneshAmpawong Sumate - p38γ and p38δ (p38γ/p38δ) have emerged as important regulators of immune function; however, their specific contribution to adaptive humoral responses remains poorly understood. Based on previous evidence that global p38γ/p38δ deficiency impairs antibody production, we investigated the T cell-intrinsic role of these kinases using conditional knockout mouse models. T cell-specific combined deletion of p38γ and p38δ altered antigen-specific IgG subclass production , causing transient reductions in IgG2b and IgG3 and a persistent decrease in IgG2a titres. This defect correlated with impaired activation of CD4 T cells, reduced generation of effector T cells, and a significant decrease in T follicular helper (Tfh) cell differentiation. Gene expression analyses revealed diminished levels of key Tfh-associated cytokines, including , , , and . Together, these findings demonstrate that p38γ/p38δ signalling in T cells is essential for Tfh differentiation, cytokine production, and effective T cell-dependent humoral immunity, including the generation of class-switched IgG antibodies, particularly IgG2 subclasses. - Source: PubMed
Publication date: 2026/08/26
González-Romero DiegoDíaz-Mora EsterFajardo PilarSanz-Ezquerro Juan JoséCarrasco Yolanda RCuenda Ana