Mouse IFNr ELISA kit
- Known as:
- Mouse IFNr Enzyme-linked immunosorbent assay test reagent
- Catalog number:
- BEK1081
- Product Quantity:
- 96 T
- Category:
- Elisa Kits
- Supplier:
- Biospect
- Gene target:
- Mouse IFNr ELISA kit
Related genes to: Mouse IFNr ELISA kit
- Gene:
- IFNR NIH gene
- Name:
- interferon production regulator
- Previous symbol:
- -
- Synonyms:
- -
- Chromosome:
- 16
- Locus Type:
- unknown
- Date approved:
- 1986-01-01
- Date modifiied:
- 2011-02-24
Related products to: Mouse IFNr ELISA kit
Related articles to: Mouse IFNr ELISA kit
- Trisomy 21 (T21) results in Down syndrome (DS), a condition associated with a high prevalence of pulmonary complications. Pulmonary hypertension (PH) is a significant comorbidity in individuals with T21. Inflammation is a well-established driver of PH, and growing evidence implicates platelets as active contributors to inflammatory-mediated pulmonary vascular disease and PH. In T21, increased interferon (IFN) signaling resulting from an additional IFN receptor gene locus contributes to immune dysregulation, and interactions between platelet activation and IFN signaling may promote thromboinflammatory pathways associated with vascular disease. To determine whether platelet activation is altered in T21, we first measured platelet activation by flow cytometry in individuals with T21 and age-matched controls. We then utilized the Dp16 mouse model of down syndrome to investigate IFN-dependent mechanisms. WT, Dp16, and Dp162xIfnrs mice 7-9 weeks of age were exposed to 10% hypobaric hypoxia for 3 or 21 days or remained at Denver altitude. Platelet activation was measured by flow cytometry. Lungs were collected to measure PF4 by ELISA and lung platelets by IHC. Vascular remodeling was measured by IHC staining of muscularized small vessels. PH was measured by RSVP and RV hypertrophy (RVH). Baseline and agonist-induced platelet activation were increased in individuals with T21, as evidenced by elevated platelet P-selectin expression and activated αIIbβ3. To investigate the immunoregulatory mechanisms underlying T21-associated PH, we utilized the Dp16 mouse model of Down syndrome in a chronic hypoxia model of PH. Consistent with our human findings, baseline, agonist-induced, and hypoxia-induced P-selectin and αIIbβ3 activation were elevated in Dp16 mice compared with wild-type (WT). Circulating PF4 and soluble GPVI were elevated at baseline and PF4 was further increased in hypoxic Dp16 mice. Lung PF4 levels were also increased at baseline and further elevated with hypoxia in Dp16 mice, despite comparable numbers of lung platelets. Dp16 mice demonstrated increased baseline pulmonary vascular remodeling, right ventricular systolic pressure (RVSP), and right ventricular hypertrophy (RVH) with both RVSP and RVH being further exacerbated in hypoxic Dp16 mice. Normalization of copy number attenuated hypoxia-induced platelet activation and lung PF4 accumulation. Normalization of copy number corrected the baseline increase in pulmonary vascular remodeling and restored RVSP to WT levels. RVH remained elevated at baseline and following hypoxia in Dp16 mice, indicating that signaling does not fully account for cardiopulmonary phenotypes associated with PH. Together, these findings demonstrate that IFN signaling contributes to platelet activation and pulmonary vascular remodeling in Dp16 mice, but does not drive PH severity, suggesting additional mechanisms in the development of T21-associated PH. This work provides novel insight into the role of IFN signaling and platelet activation in Down syndrome -associated pulmonary vascular disease and has potential clinical relevance given the presence of platelet activation in individuals with T21. - Source: PubMed
Publication date: 2026/05/22
Posey Janelle NJordan MariahOlsen-Dufour AmandaNguyen Thi-Tina NFarrell ChristineLewis Caitlin VArchambault Jamie LSul ChristinaColon-Hidalgo DanielNozik Eva SEspinosa Joaquin MSullivan Kelly DDelaney Cassidy - Pancreatic cancer, recognized as a refractory tumor, has an overall survival rate of less than 10%, and its mortality rate continues to rise. Due to the low immune activity induced by its unique tumor microenvironment, pancreatic cancer is classified as a "cold" tumor and is insensitive to current immunotherapies. However, little is still known about the identification and functional mechanisms of key regulatory molecules in the formation of "cold" tumors. - Source: PubMed
Publication date: 2025/11/24
Huang FuxinZhang ZhongyanFang JikeChen YueWei JinhuiLi QuanzhangZhang ChuanzhaoHuang ShanzhouHou Baohua - Interleukin 18 receptor 1 (IL18R1) is involved in the pathogenesis of asthma and atopic phenotypes. However, IL18R1 expression level in induced sputum supernatant of asthma remains unclear. - Source: PubMed
Publication date: 2025/08/09
Liang YuxiaYang WeiqiWang XiZong WeifengTang KunLi YueCheng Zhe - We investigate the long-term impact of repeated COVID-19 vaccinations on adaptive immunity through a 3-year study of 78 individuals without reported symptomatic infections. We observe distinct dynamics in spike-specific responses across multiple vaccine doses. While antibody levels increase and stabilize with each booster, T cell responses quickly plateau and remain stable. Notably, approximately 30% of participants show evidence suggestive of asymptomatic infections. Single-cell RNA sequencing reveals a diverse and stable landscape of spike-specific T cell phenotypes without signs of exhaustion or functional impairment. Individuals with evidence of asymptomatic infection display increased frequencies of Th17-like CD4 T cells and GZMKhi/IFNR CD8 T cell subsets. In this group, repeated vaccinations correlate with an increase in regulatory T cells, potentially indicating a balanced immune response that may mitigate immunopathology. By regularly stimulating T cell memory, boosters contribute to a stable and enhanced immune response, which may provide better protection against symptomatic infections. - Source: PubMed
Publication date: 2025/06/26
da Silva Antunes RicardoFajardo-Rosas VicenteYu Esther DawenGálvez Rosa IselaAbawi AdamEscarrega E AlexandarMartínez-Pérez AmparoJohansson EmilGoodwin BenjaminFrazier AprilDan Jennifer MCrotty ShaneSeumois GrégoryWeiskopf DanielaVijayanand PanduranganSette Alessandro - The long-term effects of repeated COVID-19 vaccinations on adaptive immunity remain incompletely understood. Here, we conducted a comprehensive three-year longitudinal study examining T cell and antibody responses in 78 vaccinated individuals without reported symptomatic infections. We observed distinct dynamics in Spike-specific humoral and cellular immune responses across multiple vaccine doses. While antibody titers incrementally increased and stabilized with each booster, T cell responses rapidly plateaued, maintaining remarkable stability across CD4+ and CD8+ subsets. Notably, approximately 30% of participants showed CD4+ T cell reactivity to non-Spike antigens, consistent with asymptomatic infections. Single-cell RNA sequencing revealed a diverse landscape of Spike-specific T cell phenotypes, with no evidence of increased exhaustion or significant functional impairment. However, qualitative changes were observed in individuals with evidence of asymptomatic infection, exhibiting unique immunological characteristics, including increased frequencies of Th17-like CD4+ T cells and GZMKhi/IFNR CD8+ T cell subsets. Remarkably, repeated vaccinations in this group were associated with a progressive increase in regulatory T cells, potentially indicating a balanced immune response that may mitigate immunopathology. By regularly stimulating T cell memory, boosters contribute to a stable and enhanced immune response, which may provide better protection against symptomatic infections. - Source: PubMed
Publication date: 2025/01/09
da Silva Antunes RicardoFajardo-Rosas VicenteYu Esther DawenGálvez Rosa IselaAbawi AdamAlexandar Escarrega EMartínez-Pérez AmparoJohansson EmilGoodwin BenjaminFrazier AprilDan Jennifer MCrotty ShaneSeumois GrégoryWeiskopf DanielaVijayanand PanduranganSette Alessandro