Anti-Human CD132 PE 100 tests
- Known as:
- Antibody toHuman CD132 PE 100 tests
- Catalog number:
- 12-1329-42
- Category:
- -
- Supplier:
- eBioscience
- Gene target:
- Anti-Human CD132 100 tests
Related genes to: Anti-Human CD132 PE 100 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 100 tests
Related articles to: Anti-Human CD132 PE 100 tests
- Monocytic acute myeloid leukemia (AML) is an aggressive malignancy associated with poor prognosis. High expression levels of LILRB3 and LILRB4 are commonly observed in monocytic AML. In this study, the expression of LILRB3 and LILRB4 was analyzed in monocytic AML patient samples, leukemic stem cell-enriched populations, and AML cell lines, revealing frequent co-expression and suggesting that a dual-targeting approach may provide enhanced therapeutic benefit. Accordingly, dual-targeting chimeric antigen receptor (CAR)-T cells were engineered using a single-chain variable fragment (scFv) derived from a humanized antibody capable of recognizing both LILRB3 and LILRB4. In vitro, LILRB3/4 CAR-T cells exhibited potent, antigen-dependent cytotoxicity against AML cell lines and primary blasts with minimal toxicity to normal hematopoietic stem/progenitor cells. Additionally, these CAR-T cells induced superior lysis of double-positive leukemic cells compared with single-positive populations. In both subcutaneous and systemic AML xenograft models, treatment with LILRB3/4 CAR-T cells significantly reduced tumor burden and prolonged survival. Collectively, these results demonstrate that LILRB3/4 CAR-T cells represent a promising therapeutic strategy for monocytic AML. Abbreviations: AML, Acute myeloid leukemia; BLI, Biolayer interferometry; B-NDG, NOD.CB17-Prkdc Il2rg/Bcgen; CAR-T, Chimeric antigen receptor T cell; CFSE, Carboxyfluorescein succinimidyl ester; CRS, Cytokine release syndrome; ELISA, Enzyme-linked immunosorbent assay; E:T ratio, Effector-to-target ratio; FAB, French-American-British; GM-CSF, Granulocyte-macrophage colony-stimulating factor; HSPCs, Hematopoietic stem and progenitor cells; IFN-γ, Interferon-gamma; IL-1, Interleukin-1; IL-2, Interleukin-2; IL-6, Interleukin-6; IL-7, Interleukin-7; IL-15, Interleukin-15; ITIMs, Immunoreceptor tyrosine-based inhibitory motifs; K, Equilibrium dissociation constant; LILRB, Leukocyte immunoglobulin-like receptor B; LILRB3, Leukocyte immunoglobulin-like receptor B3; LILRB4, Leukocyte immunoglobulin-like receptor B4; LSC, Leukemia stem cell; Luc, Luciferase; M4, Acute myelomonocytic leukemia; M5, Acute monocytic leukemia; MDSCs, Myeloid-derived suppressor cells; NCG, NOD/ShiLtJGpt-PrkdcIl2rg/Gpt; PBMCs, Peripheral blood mononuclear cells; PBS, Phosphate buffered saline; R/R, Relapsed/refractory; scFv, Single-chain variable fragment; SD, Standard deviation; SPF, Specific pathogen-free; SPR, Surface plasmon resonance; STAR-T, Synthetic T cell receptor and antigen receptor-T therapy; TCGA, The Cancer Genome Atlas; TNF-α, Tumor necrosis factor-alpha; TPM, Transcripts per million; VH, Variable region sequences of the heavy; VL, Variable region sequences of the light. - Source: PubMed
Publication date: 2026/07/11
Chen XiaofengGuo CuiyuTu YongyanWei XianRen QiannanYu HongbinDeng HanWu JialinChen TianZhang ZhixiongHu ZhongguoZhao ShengyanZhang GuangbingLai QinhuaiYang ShuyunZhang YingluCui SusuJiang XiaohuaZhang RuiruiWang DoudouLi DonghaoLiu HuayiGou LantuYang Jinliang - 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
Publication date: 2026/06/23
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
Publication date: 2026/05/12
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