Anti-Human CD132 PE 25 tests
- Known as:
- Antibody toHuman CD132 PE 25 tests
- Catalog number:
- 12-1329-41
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD132 25 tests
Ask about this productRelated genes to: Anti-Human CD132 PE 25 tests
- Gene:
- IL2RG NIH gene
- Name:
- interleukin 2 receptor subunit gamma
- Previous symbol:
- SCIDX1, IMD4, CIDX
- Synonyms:
- CD132
- Chromosome:
- Xq13.1
- Locus Type:
- gene with protein product
- Date approved:
- 1992-11-30
- Date modifiied:
- 2019-04-23
Related products to: Anti-Human CD132 PE 25 tests
Related articles to: Anti-Human CD132 PE 25 tests
- Systemic lupus erythematosus (SLE) has a significant female bias; however, it remains unclear whether X-chromosomal dysregulation increases the risk in females. Furthermore, while the role of X-linked genes in SLE pathogenesis is recognised, the analysis of genetic risks in SLE has largely focussed on autosomal genes. - Source: PubMed
Publication date: 2026/06/30
Gray Lachlan GTelfser AidenHu HannahKane AlisaDeenick Elissa KPhan Tri GiangBallouz Sara - Acute myeloid leukemia (AML) remains a therapeutic challenge due to drug resistance and relapse, which are often driven by the protective bone marrow (BM) niche. Conventional xenograft models fail to adequately recapitulate this niche-specific pathophysiology. To overcome this limitation, a novel magnetically targeted intramedullary (MagIC-TI) xenograft model was developed. Magnetically labeled doxorubicin (DOX)-resistant HL60 cells (Mag-Re) were injected into the femurs of NSG (nonobese diabetic [NOD] Cg-PrkdcIL2rg/SzJ) mice using a patented microinjection syringe under localized magnetic guidance. With the MagIC-TI model, rapid (day 1) and specific (100% by day 7) leukemic engraftment was achieved within the femoral BM, whereas intravenous (IV) injection led to delayed (mean 23.67 ± 10.26 days) and disseminated engraftment. Bioluminescence imaging, histopathological analysis, flow cytometry, and molecular assays confirmed that disease was localized in the MagIC-TI model. In contrast, extramedullary infiltration, predominantly in the lungs, spleen, liver, and kidneys, was observed early in progression in the IV model. The MagIC-TI model discriminated drug responses, showing effective tumor burden reduction with homoharringtonine (HHT) and unequivocal DOX resistance, a distinction that was obscured in heterogeneous IV models. Furthermore, employing a semisolid decalcification (SSD) system preserved green fluorescent protein (GFP) fluorescence, enabling high-resolution visualization of engrafted cells within bone tissue. The MagIC-TI model enables BM-targeted, rapid, and efficient leukemic engraftment and allows discrimination of drug sensitivity and resistance. This model provides a robust and reproducible platform for modeling the leukemia BM niche and for preclinical evaluation of niche-directed therapies. - Source: PubMed
Mai QiusuiLiu TaosongTang LuxiaDai LihanLi SiyiGuo JingyiXia WenChen LingxiWu JiabaoRong JiaweiZhang WeishenZhang JiaxingXu XiaojunJiang Qianli - Zika virus (ZIKV) infections have been linked to severe neurological disorders, including microcephaly and Guillain-Barré syndrome in humans as well as mouse models of ZIKV infection. Despite the association, the mechanisms underlying ZIKV-induced neuropathology remain incompletely understood. We have recently shown that antigen independent CD8 T cells mediate neurological disease in ZIKV-infected mice independent of the amount of infectious virus in the CNS. To further investigate the role of brain viral load and lymphocytes in ZIKV infection we studied the viral kinetics, pathology, and immune responses of ZIKV-infected NOD-Rag1Il2rg mice, which are deficient in lymphoid cells. Despite prolonged high viral titers in the brain, NOD-Rag1IL2rg mice did not develop neurological symptoms following ZIKV infection, contrasting with the infection outcomes of Ifnar1 mice which exhibit paralysis despite lower viral load. Notably, we observed significant differences in brain myeloid cells in the presence or absence of lymphoid cells. While Ifnar1 mice showed robust infiltration of CD45CD11b cells in the brain, lymphocyte-deficient NOD-Rag1IL2rg mice exhibited reduced recruitment and activation of these cells. Additionally, we found that CD45CD11b cells displayed a more inflammatory phenotype in Ifnar1 mice compared to NOD-Rag1IL2rg mice. Our study highlights the complex interplay between the immune system and viral infection in ZIKV-induced neuropathology and underscores the importance of considering immune responses in the development of therapeutic interventions for ZIKV. - Source: PubMed
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Montemarano AmeliaBalint ElizabethAshkar Ali A - To report the clinical impact of structured hospital-based dental management as an adjunct to systemic antifungal therapy in refractory oral candidiasis in Severe Combined Immunodeficiency (SCID). - Source: PubMed
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Delgado Renata Zoraida RizentalPastorino Antônio CarlosFranco Juliana Bertoldi - Relapse and graft-versus-host disease (GvHD) remain primary causes of treatment failure in patients with B-cell acute lymphoblastic leukemia (B-ALL) undergoing allogeneic hematopoietic cell transplantation (allo-HCT). While abatacept (ABATA) effectively mitigates GvHD via CD28-costimulation blockade, there is significant concern that it concurrently diminishes graft-versus-leukemia (GvL) effects, potentially leading to higher relapse rates. We investigated whether blinatumomab (BLINA) retains antileukemic efficacy in the presence of ABATA using in vitro assays and humanized NOD.Cg-Prkdc Il2rg Tg(IL15)1Sz/SzJ (NSG-IL15) and NOD.Cg-Prkdc Il2rg/SzJ (NSG) mouse models. - Source: PubMed
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