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TLR9 deficiency promotes CD73 expression in T cells and diabetes protection in NOD mice

ABSTRACT: Analyze the effect of TLR9 deficiency on immue cell function at the gene expression level. Our hypothesis was that TLR9 deficiency promotes CD73 expression in T cells thus regulates autoimmune diabetes development in NOD mice. Sorted TCRb+ cells were pooled from several mice for furhter RNA extraction and cRNA labeling.

ORGANISM(S): Mus musculus

SUBMITTER: NINGWEN TAI

PROVIDER: E-GEOD-48781 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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TLR9 deficiency promotes CD73 expression in T cells and diabetes protection in NOD mice

Project description:Analyze the effect of TLR9 deficiency on immue cell function at the gene expression level. Our hypothesis was that TLR9 deficiency promotes CD73 expression in T cells thus regulates autoimmune diabetes development in NOD mice.

2013-07-11 | GSE48781 | GEO

Cell intrinsic expression of TLR9 in autoreactive B cells constrains BCR/TLR7-dependent responses

Project description:Endosomal Toll-like receptors (TLRs) play an important role in the etiology of systemic autoimmune diseases such as SLE, where DNA- and RNA-associated autoantigens activate autoreactive B cells through TLR9- and TLR7-dependent pathways, respectively. Nevertheless, TLR9-deficient autoimmune prone mice develop more severe clinical disease, while TLR7-deficient and TLR7/9-double deficient autoimmune-prone mice develop less severe disease. To determine whether the regulatory activity of TLR9 is B cell intrinsic, we have now directly compared the functional properties of autoantigen activated WT, TLR9-deficient and TLR7-deficient B cells, in an experimental system where proliferation depends on BCR/TLR co-engagement. In vitro, TLR9-deficient cells are less dependent on survival factors for a sustained proliferative response than either WT or TLR7-deficient cells. The TLR9-deficient cells also preferentially differentiate toward the plasma cell lineage, as indicated by expression of CD138, sustained expression of IRF4, and other molecular markers of plasma cells. In vivo, autoantigen-activated TLR9-deficient cells give rise to greater numbers of autoantibody producing cells. Our results identify distinct roles for TLR7 and TLR9 in the differentiation of autoreactive B cells that explain the capacity of TLR9 to limit, and TLR7 to promote, the clinical features of SLE. AM14 WT, Tlr7-/-, Tlr9-/- and Tlr7/9-/- B cells were stimulated with PL2-3 for 0, 6, 24, and 42 hours, for a total of 16 samples.

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ATAC-seq analysis of aged-associated B cells (ABC) across three TLR9 genotypes (TLR9WT, TLR9-/- and non-signaling TLR9P915H/P915H) isolated from a mixed chimeric setting in the MRL/lpr murine model of systemic lupus erythematosus.

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IRF-5 and IRF-8 govern the response of Human Plasmacytoid Dendritic Cells following TLR9 ligation

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2016-06-01 | E-GEOD-70429 | biostudies-arrayexpress

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2024-04-11 | GSE263396 | GEO

RNA-seq analysis of follicular (FO), marginal zone (MZ) and aged-associated B cells (ABC) across three TLR9 genotypes (TLR9WT, TLR9-/- and non-signaling TLR9P915H/P915H) isolated from a mixed chimeric setting in the MRL/lpr murine model of SLE

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Project description:We report the application of single-molecule-based sequencing technology for mapping the Egr2 transcriptional program in developing thymic NKT. We found that Egr2 controls the induction of genes required for NKT development. Examination of developing NKT cells and thymocytes receiving a strong TCR signal in vivo by injecting 500ug anti-TCRb antibody.

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Mus musculus

Project description:TLR9 deficiency promotes CD73 expression in T cells and diabetes protection in NOD mice

| PRJNA211749 | ENA