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Determine anti-Siglec-F and IL-33 costimulation induced transcriptional changes on murine eosinophils

ABSTRACT: Eosinophils costimulation with anti-Siglec-F and IL-33 synergistically increases their IL-4 and IL-13 release (Willebrand et al. PLoS One 2016). Here we analyze costimulation induced transcriptional changes involved that potentially enhance effector release.

ORGANISM(S): Mus musculus

PROVIDER: GSE166968 | GEO | 2021/11/23

REPOSITORIES: GEO

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Determine anti-Siglec-F and IL-33 costimulation induced transcriptional changes on murine eosinophils

Project description:Determine anti-Siglec-F and IL-33 costimulation induced transcriptional changes on murine eosinophils

| PRJNA702493 | ENA

Siglec-F+ neutrophils in the spleen induce immunosuppression following acute infection

Project description:The mechanisms underlying the increased mortality of secondary infections during the immunosuppressive phase of sepsis remain elusive. We established a mouse model of sepsis-induced immunosuppression followed by secondary infection. Compared to other organs, we observed a significant reduction in pro-inflammatory cytokines in the spleen, accompanied by a marked increase in IL-10 production, primarily by infiltrating neutrophils. Furthermore, we confirmed that these infiltrating neutrophils in the spleen during the immunosuppressive phase of sepsis undergo phenotypic change in the local microenvironment, exhibiting high expression of neutrophil biomarkers such as Siglec-F, Ly6G, and Siglec-E. These neutrophils subsequently produced IL-10 to suppress T lymphocytes. Depletion of neutrophils or specifically targeting Siglec-F leads to a notable improvement in the survival of mice with secondary infections. The identification of Siglec-F+ neutrophils as key regulators of immunosuppression following sepsis represents a novel finding with potential therapeutic implications.

2024-04-24 | GSE264139 | GEO

Gene expression in eosinophils from IL-5 transgenic mice

Project description:Dr. Paulson's group investigates the roles of carbohydrate-binding proteins involved in immune regulation and human disease, through their interaction with carbohydrate groups expressed on cell surface glycoconjugates. This laboratory is currently focused on how sialoside ligands modulate Siglec functions and on understanding the molecular basis of glycosylation changes following differentiation and activation of leukocytes. Three RNA preparations from IL-5 transgenic C567/B1 adult mouse eosinophils were sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays. Data was analyzed to determine glycosyltransferase expression on mouse eosinophils, with specific interest in a cis-ligand of Siglec-F on eosinophils

2011-04-29 | E-GEOD-28923 | biostudies-arrayexpress

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

IL-6 blockade prevents costimulation blockade-resistant allograft rejection by promoting intragraft regulation in T cell-depleted recipients [GIL]

Project description:The efficacy of costimulation blockade (CTLA4Ig/belatacept) in transplantation is reduced by an increased incidence of T cell-mediated rejection, which also persists after induction therapy with anti-thymocyte globulin (ATG). Herein, we investigate why ATG fails to prevent costimulation blockade-resistant rejection and how this barrier can be overcome. ATG did not prevent graft rejection in a murine heart transplant model of CTLA4Ig therapy and induced a pro-inflammatory cytokine environment. While ATG improved the balance between Tregs and effector T cells in the peripheral compartment, it had no such effect within cardiac allografts, which showed signs of inflammation. Neutralizing IL-6 alleviated inflammation, increased intragraft Treg frequencies long-term, and enhanced intragraft IL-10 and Th2 cytokine expression. IL-6 blockade together with ATG led to long-term, rejection-free heart graft survival under CTLA4Ig therapy. Combining ATG with IL-6 blockade prevents costimulation blockade-resistant rejection, thereby eliminating a major impediment to clinical use of costimulation blockers in transplantation.

2024-04-21 | GSE241471 | GEO

IL-6 blockade prevents costimulation blockade-resistant allograft rejection by promoting intragraft regulation in T cell-depleted recipients [FFPE]

2024-04-21 | GSE241470 | GEO

Global chromatin accessibility of gene locus in CD4+ T cells activated with or without OX40 costimulation

Project description:OX40 is a T cell costimulatory molecule in the tumor necrosis factor receptor (TNFR) superfamily. Unlike other costimulatory molecules, OX40 is not expressed by naive T cells, but its expression is rapidly induced following T cell activation, and OX40 costimulation plays a critical role in cell survival, proliferation, and generation of memory cells. We used ATAC-seq to detail the chromatin accessibility of gene locus of activated CD4 T cells with or without OX40 costimulation in the presence of TGF-β1 and IL-2 and identified distinct classes of genes after OX40 costimulation.

2018-05-18 | GSE114568 | GEO

Tuberculosis-associated IFN-I induces Siglec-1 on microtubule-containing tunneling nanotubes and favors HIV-1 spread in macrophages

Project description:To understand the susceptbility of human M(IL-10) macrophages to human immunodeficiency virus, we performed a genome-wide transcriptome analysis in these cells to identify a gene profile responsible for this phenomenon. A distinct 60 gene-transcript signature was defined in M(IL-10) macrophages, using a combination of the expression level, statistical filters and hierarchical clustering; 51 genes were up-regulated and 9 genes were down-regulated in M(IL-10) macrophages compared to control cells. Among the genes upregulated, we identified a interferon-stimulated gene (ISG) signature include SIGLEC-1. We confirmed SIGLEC-1 and other five ISG genes by qPCR, FACS and western blot.

2020-04-04 | GSE139511 | 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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