Ask about this productRelated genes to: SIGLEC9 antibody
- Gene:
- SIGLEC9 NIH gene
- Name:
- sialic acid binding Ig like lectin 9
- Previous symbol:
- -
- Synonyms:
- CD329
- Chromosome:
- 19q13.3-q13.4
- Locus Type:
- gene with protein product
- Date approved:
- 2000-03-29
- Date modifiied:
- 2016-01-20
Related products to: SIGLEC9 antibody
Related articles to: SIGLEC9 antibody
- Over the past decade, positron emission tomography (PET) has become an important part of the management of large-vessel vasculitis (LVV). Current clinical practice relies predominantly on [18F]fluorodeoxyglucose ([18F]FDG) PET combined with computed tomography (CT) for anatomical localisation. Although [18F]FDG PET/CT shows high specificity and good sensitivity for primary diagnosis, persistent vascular uptake during clinical remission limits its specificity for relapse assessment and complicates longitudinal monitoring. Alongside technological advances in PET hardware, an expanding portfolio of alternative radiotracers has emerged to probe more specific inflammatory pathways and cell-associated processes.This narrative review summarises the most informative clinical evidence currently available for novel PET tracers in giant cell arteritis (GCA) and Takayasu's arteritis (TAK). Targets related to immune cell recruitment and vascular inflammation include the vascular adhesion protein-1 (VAP-1)/sialic-acid-binding immunoglobulin-like lectin-9 (Siglec-9) axis, assessed by [68Ga] Ga-DOTA-Siglec-9. Similarly, C-X-C chemokine receptor 4 (CXCR4) imaging with [68Ga]PentixaFor has been explored as an approach to capture chemokine-mediated immune cell trafficking. For the assessment of myeloid activation, somatostatin receptor subtype 2 (SSTR2) imaging using [68Ga] DOTATATE or [18F]FET-βAG-TOCA has been explored as an approach to differentiate active from inactive disease. Imaging of the 18 kDa translocator protein (TSPO), a mitochondrial outer membrane protein associated with cellular stress and myeloid activation, seeks to provide a complementary inflammation- and stress-related read-out, although its clinical applicability is influenced by ligand-specific performance and genotype-dependent binding. Finally, fibroblast activation protein (FAP)-targeted PET with fibroblast activation protein inhibitors (FAPI, e.g. [68Ga]-FAPI-46) has been investigated to visualise fibroblast activation and vascular remodelling, with persistent uptake during clinical remission potentially indicating ongoing tissue repair or structural remodelling. - Source: PubMed
Publication date: 2026/04/22
Petzinna Simon MBauer Claus-JürgenSchäfer Valentin S - Sorafenib is the first-line therapy for advanced hepatocellular carcinoma (HCC). However, acquired resistance to sorafenib remains a significant challenge. Previous studies have shown that sorafenib treatment induces the formation of truncated O-glycans in HCC cells, but the relationship between sorafenib-induced glycosylation changes and acquired therapy resistance remains unclear. Primary natural killer (NK) cells, freshly isolated from peripheral blood or following culture and expansion, expressed the glycoimmune checkpoints Siglec-7 and Siglec-9. HCC cells exhibited varying levels of Siglec-7/9 ligands on their surface. Sorafenib-resistant liver cancer cells displayed hypersialylation, leading to increased expression of surface Siglec-7/9 ligands, which conferred protection against NK cell-mediated cytotoxicity. Silencing ST3GAL1 significantly reduced Siglec-7 ligand expression on liver cancer cells, enhancing their susceptibility to NK-mediated cytotoxicity and cetuximab-induced antibody-dependent cellular cytotoxicity (ADCC) in epidermal growth factor receptor (EGFR)-expressing tumor cells. Furthermore, high ST3GAL1 expression correlated with poor clinical outcomes in patients with stage 1-2 HCC. This study highlights the critical role of ST3GAL1 in regulating Siglec-7 ligands to facilitate immune escape from NK cell cytotoxicity. Moreover, its elevated expression is associated with adverse clinical outcomes in HCC. Targeting ST3GAL1 may represent a promising strategy to enhance NK cell-mediated anti-tumor immunity in HCC. - Source: PubMed
Publication date: 2026/04/10
Fan Tan-ChiHung Tsai-HsienYeh Chau-TingLin Po-TingChang Nai-ChuanLo Tzu-ChiWu Tsai-JungYu JohnYu Alice L - Macrophages exert antitumorigenic activity through phagocytosis, but phagocytosis-enhancing therapeutics have not improved acute myeloid leukemia (AML) outcomes. To identify phagocytosis regulators, we performed CRISPR knockout screens in human AML cells cocultured with human macrophages. We found that the "don't eat me" signal CD47 inhibited mouse but not human macrophage phagocytosis. However, O-linked glycosylation and sialylation were strong negative regulators of phagocytosis. In AML, the cell surface mucin-like glycoprotein CD43 was the major effector of these pathways. Inhibition of phagocytosis by CD43 was dependent on the length of its ectodomain and independent of the macrophage sialic acid receptors SIGLEC-1, SIGLEC-7, and SIGLEC-9. The inhibitory effects of CD43 extended beyond human macrophages to natural killer and T cells. Thus, CD43 forms a glyco-immune barrier that restrains both innate and adaptive antileukemic immunity. - Source: PubMed
Publication date: 2026/04/09
Chung JoohoVallurupalli MounicaNoel SarahSchor GailMrowka SofiaScapozza IlarioDemere ZelalemKammula Sachin VHu MargaretKim Sarah YLiu YuhJongNobrega CelestePerera Jonathan JWrona EwaCheruiyot Collins KLin YunkangWu David WSaberi MariaCruickshank AidanWoods Elliot CChuong Cun LanBirocchi FilippoKammula Ashwin VAvila Omar IKnudsen NelsonKocak MustafaDoench John GProcter DeanThornton LindseyBrunner Andrew MWiner EricDeAngelo Daniel JGarcia Jacqueline SStone Richard MJenkins Russell WMaus Marcela VGraubert Timothy AYates Kathleen BGolub Todd RManguso Robert T - Nucleic acid vaccines (DNA and mRNA) induce immunity by driving in situ antigen expression in host cells. For non-viral pathogens, however, host expression can impose post-translational modifications absent from the native microbial antigen. Tuberculosis (TB) remains a leading cause of infectious mortality, and nucleic acid vaccines targeting the Mycobacterium tuberculosis antigen 85 (Ag85) complex did not confer protective efficacy in clinical trials. We hypothesized that host-derived N-glycosylation of Ag85 immunogens expressed in mammalian cells compromises immune recognition. Here, we define structural, biochemical and immunological mechanisms by which host-imposed N-glycosylation remodels a bacterial antigen expressed in mammalian cells. We show that Ag85B expressed in human Expi293 cells is microheterogeneously N-glycosylated at four canonical sequons (N52, N224, N234, N280) with predominantly complex, highly fucosylated, and frequently sialylated glycans. Molecular dynamics simulations indicate that these glycans occupy substantial conformational space and reduce solvent and antibody-accessible surface area, occluding multiple established B-cell and T-cell epitope regions. Consistent with glycan-mediated shielding, mammalian-expressed Ag85B shows markedly reduced binding to an Ag85-complex monoclonal antibody by competitive ELISA and biolayer interferometry, and sialylated glycans enable Siglec-9 binding that is abrogated by sialidase treatment. Together, these findings define the structural and biochemical mechanisms by which host glycosylation can remodel bacterial vaccine antigens, supporting glycosylation-aware immunogen engineering as a design principle for nucleic acid vaccines targeting non-viral pathogens. - Source: PubMed
Publication date: 2026/04/02
Cinar Mukaddes SAdams Trevor MNawaz ZahraDemir Elif SDemirturk Mariye EKeelaghan Aidan PNazaar Shaima MRoberts Blaine ROzdilek AhmetAvci Fikri Y - The glyco-immune checkpoints Siglec-7 and Siglec-9 have received considerable interest as targets for cancer immunotherapy. How Siglec-7/9-sialic acid -interactions on immune cells influence -signaling induced by tumor cells and whether Siglec-7 and -9 co-blockade can enhance immune effector cell function are key questions for clinical translation. We developed and applied single and dual Jurkat/MA NFAT-luciferase reporter cells expressing wild-type or mutant chimeric Siglec-7 and/or -9. -interactions on these Jurkat/MA reporter cells prevented Siglec-7 and -9 signaling induced by -ligands, i.e. on tumor cells. In Jurkat/MA cells expressing both receptors, Siglec-7/9 co-inhibition was essential to fully block receptor signaling. Extrapolating our findings to human primary cells, NK cell-mediated killing of melanoma and acute myeloid leukemia (AML) cell lines and patient-derived AML cells was increased upon Siglec-7 and/or -9 blockade. Importantly, co-blockade was superior to single blocking strategies and the effects were most pronounced when -ligands were removed from the NK cell' surface using sialidase. Further diving into -ligand dynamics on primary human NK cells, physiological NK cell activation with IL-2 or IFN- or IL-15/IL-2-induced proliferation was shown to significantly downregulate Siglec-7 and -9 -ligand expression. Moreover, Siglec-7 and -9 ligands were progressively downregulated with each round of NK cell division. Taken together, our findings highlight the important role of -interactions in regulating -interactions and emphasize the potential of simultaneously blocking Siglec-7 and -9 for clinical applications. These insights may guide the design of next-generation Siglec-targeted immunotherapies. - Source: PubMed
Publication date: 2026/04/02
van Eck van der Sluijs JesperValk Anne H Cvan Houtum Eline J HKers-Rebel Esther DLooman MaaikeHobo WillemijnMarneth Anna EDolstra Harryvan den Boogaard LuneBüll ChristianCornelissen Lenneke A MAdema Gosse J