Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA319329 | ENA |
REPOSITORIES: ENA
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Project description:TLR signaling in C57BL/6J TLR7-tolerant CD3+ T-cells over B6 TLR7 null CD3+ T-cells.
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Project description:Murine CD3+ T-cells were immunomagnetically purified from the spleens of C57BL/6J mice and were pretreated in vitro for three days in the presence of R848 (5 μg/ml). Gene expression profile of wild type (WT) C57BL/6J TLR7-primed T-cells, was compared to unmanipulated B6 TLR7 null CD3+ Τ-cells. We used Qiagen Toll-like Receptor RT2 Profiler PCR Array kit to quantitate gene expression profiling of the TLR signaling pathway.
2017-04-21 | GSE80573 | GEO
Project description:TLR signaling in C57BL/6J TLR2,4,7-tolerant splenocytes over PBS-treated counterpart.
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Project description:Murine CD3+ T-cells were immunomagnetically purified from the spleens of C57BL/6J mice and were pretreated in vitro for three days in the presence of R848 (5 μg/ml). Unmanipulated T-cells served as negative control. We used Qiagen Toll-like Receptor RT2 Profiler PCR Array kit to quantitate gene expression profiling of the TLR signaling pathway.
2017-04-21 | GSE80570 | GEO
Project description:The debilitating autoimmune disease Systemic Lupus Erythematosus (SLE) is closely associated with Toll-like receptor (TLR) 7 and type I interferon (IFN) activity in humans and in murine SLE-like disease. Two central manifestations of SLE affect the myeloid lineage of the immune system, myeloid expansion and anemia. Yet, whether these symptoms are linked and the role of TLR7 and/or type I IFN in these processes is unclear. Here we show that TLR7 signaling promotes cell-autonomous, phosphoinositide 3-kinase (PI3K)- and mammalian target of rapamycin (mTOR)-dependent macrophage development from the common myeloid progenitor (CMP). Strikingly, this TLR7-driven macrophage development requires and is enhanced by type I IFN. Genome-wide transcriptional profiling and functional studies demonstrated that TLR7 promoted the expression of Spic, the master regulator of splenic red pulp macrophages (RPM) and preferential development of hemophagocytic RPM-like cells from CMP in vitro. We found increased incidence of RPM-like cells in vivo in a mouse model of SLE caused by TLR7 overexpression, which correlated with decreased red blood cell (RBC) count and anemia. These findings demonstrate a mechanism by which TLR7 signaling promotes anemia that is of clinical significance in SLE, other rheumatological diseases and chronic viral infections. This work also identifies a previously unknown molecular pathway by which TLR signaling and type I IFN synergize to promote myeloid development from hematopoietic progenitors. CMP were sorted from the bone marrow of wild-type C57BL/6 mice, cultured with SCF+R848 or SCFr+MCSF, and CD11b+F4/80+ macrophages sorted after 5 days, n=3 per group
2016-07-01 | E-GEOD-70520 | biostudies-arrayexpress
Project description:Systemic autoimmune diseases such as lupus and scleroderma are characterized by the loss of tolerance to nuclear antigens, but the mechanisms by which specific autoantibodies are selected are unclear. Here we report that B cells containing the Y-linked autoimmune accelerator (Yaa) locus are intrinsically biased towards nucleolar antigens due to a duplication of TLR genes in the pseudoautosomal region that makes them more responsive to TLR7 ligands and augments the Btk-dependent signaling pathway. These findings provide genetic evidence that naturally occurring differences in expression of TLR7 have a dramatic impact on antigen selection in autoimmunity. Follicular B cells were isolated from spleen of C57BL/6 male and C57BL/6.Yaa male. Four mice from each group using in this analysis were 2 months old. Dye swab labeled RNA had been done in one mice from each group.
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