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Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [ST]

ABSTRACT: Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [ST]

PROVIDER: PRJNA986883 | ENA |

REPOSITORIES: ENA

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Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response

Project description:Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response

| PRJNA988021 | ENA

Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [scRNA-seq]

Project description:Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [scRNA-seq]

| PRJNA986889 | ENA

Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [bulk RNA-seq]

Project description:Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [bulk RNA-seq]

| PRJNA988030 | ENA

Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [ST]

Project description:The neoadjuvant immune checkpoint blockade therapy only benefits a limited fraction of glioblastoma multiforme (GBM) patients. Thus, targeting other immunomodulators on myeloid cells is an attractive therapeutic option. Here, we performed single-cell RNA sequencing and spatial transcriptomics of GBM patients treated with neoadjuvant anti-PD-1 therapy. We identified unique monocyte-derived tumor-associated macrophage (TAM) subpopulations with functional plasticity that highly expressed the immunosuppressive SIGLEC9 gene and preferentially accumulated in the non-responders to anti-PD-1 treatment. Deletion of Siglece (murine homologue) resulted in significantly restrained tumor development and prolonged survival in mouse models. Mechanistically, targeting Siglece directly activated both CD4+ T cells and CD8+ T cells through antigen presentation, secreted chemokines and co-stimulatory factor interactions. Furthermore, Siglece deletion synergized with anti-PD-1/PD-L1 treatment to improve antitumor efficacy. Our data demonstrated that Siglec-9 is an immune checkpoint molecule on macrophages that can be targeted to enhance anti-PD-1/PD-L1 therapeutic efficacy for GBM treatment.

2023-06-29 | GSE235672 | GEO

Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [scRNA-seq]

2023-06-29 | GSE235676 | GEO

Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response [bulk RNA-seq]

2023-06-29 | GSE235911 | GEO

Type-I interferon inducible genes 26 weeks after mCMV infection in Siglec-H wt and Siglec-H ko mice and their non infected controls

Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-Î± in vitro and that Siglec-H ko mice produce more IFN-Î± after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease. For microarray experiments gene expression profiles of total splenic cells from two wt and Siglec-H ko mice 26 weeks after infection with luciferase expressing murine Cytomegalovirus (5x105 pfu) or from two uninfected wt and Siglec-H ko control mice were analyzed

2016-03-16 | E-GEOD-79248 | biostudies-arrayexpress

Siglec-9 acts as an immune checkpoint molecule on macrophages in glioblastoma, restricting T cell priming and immunotherapy response

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-06-29 | GSE235913 | GEO

Effect of soluble Siglec-14 on macrophage polarization

Project description:Influence of soluble Siglec-14 on macrophage poloarization was examined by analyzing the transcripts from human macrophages cultured in the presence or absence of recombinant soluble Siglec-14 protein

2018-10-29 | GSE121311 | GEO

Type-I interferon inducible genes 26 weeks after mCMV infection in Siglec-H wt and Siglec-H ko mice and their non infected controls

Project description:Type I interferons are critical anti-viral cytokines during virus infections and have also been implicated in the pathogenesis of systemic lupus erythematosus (SLE). The secretion of type I interferon of pDCs is modulated by Siglec-H, a DAP12 associated receptor on pDCs. We showed that Siglec-H deficient pDCs produce more of the type I interferon IFN-α in vitro and that Siglec-H ko mice produce more IFN-α after murine cytomegalovirus (mCMV) infection in vivo, leading to efficient clearance of the virus. Furthermore, ageing Siglec-H ko mice showed a mild form of systemic autoimmunity. In contrast, Siglec-H ko mice developed a severe form of systemic lupus-like autoimmune disease with strong kidney nephritis several weeks after a single mCMV infection. This induction of systemic autoimmune disease after virus infection in Siglec-H ko mice was accompanied by a type I interferon signature and fully dependent on type I interferon signaling. These results show that Siglec-H normally serves as modulator of type I interferon responses after infection with a persistent virus and thereby prevents induction of autoimmune disease.

2016-03-16 | GSE79248 | GEO

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