WT and NLRP6 KO CD103+ and CD103- B cell expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE224472 | GEO | 2023/02/08
REPOSITORIES: GEO
Similar Datasets
Project description:Mouse lung CD11c+ dendritic cells are composed of 2 major DC subsets, the CD103+CD11b-low/intermediate DC (CD103+ DC) and the CD11b-highCD103- DC (CD11b-high DC). These 2 subsets are functionally distinct. Comparison of their functions showed CD103+ DC Microarray analysis was performed to compare the gene expression profiles of the 2 lung DC subsets in naïve mice. Perfused lungs from 6-8-week naïve BALB/cByJ mice were pooled and digested with collagenase D. CD11c+ cells were selected by anti-CD11c magnetic microbeads (Miltenyi) and stained by fluorochrome-conjugated mAb against I-A, CD103, CD11b, and CD11c plus 7-
2010-03-24 | E-GEOD-17322 | biostudies-arrayexpress
Project description:Mouse lung CD11c+ dendritic cells are composed of 2 major DC subsets, the CD103+CD11b-low/intermediate DC (CD103+ DC) and the CD11b-highCD103- DC (CD11b-high DC). These 2 subsets are functionally distinct. Comparison of their functions showed CD103+ DC Microarray analysis was performed to compare the gene expression profiles of the 2 lung DC subsets in naïve mice.
2010-03-15 | GSE17322 | GEO
Project description:We hypothesize that under homeostatic as well as inflammatory conditions circulating monocytes and/or their bone marrow-derived progenitors might contribute to the replenishment of CD103+ and CD103- DC in lymphoid and non-lymphoid compartments. To that end, bone marrow cells from CX3CR1+/gfp C57BL/6 mice were sorted as follows: lineage negative (CD3, CD19, NK1.1, Ter119, Ly6G and CD11c) CX3CR1+c-kit+. Sorted cells were further cultured in vitro under the continuous presence of GM-CSF. lin-CX3CR1+c-kit+ bone marrow cells gave rise to CD103+ and CD103- DC in vitro. To test whether CD103 might be a suitable marker that allows the differentiation of functionally distinct DC subsets generated in vitro, CD11c+CD103+ and CD11c+CD103- DC were sorted from day 5 cultures of lin-CX3CR1+c-kit+ cells and analyzed by whole mouse genome microarrays from Agilent technologies. Compared to CD103+ DC, CD103- DC displayed a strong up-regulation of transcripts for genes involved in innate immunity, whereas those involved in costimulation were down-modulated. Our data suggest distinct functional activity of these two DC subsets. Keywords: Transcriptional profiling-Cell type comparison We compared the transcriptional profile of CD11c+CD103+ and CD11c+CD103- dendritic cells by use of Agilent Whole Mouse Genome Microarrays. Two sets of samples were generated independently as real biological replicates. The microarray analysis was performed as a dual-color experiment, including a dye-swap.
2008-12-17 | E-GEOD-10882 | biostudies-arrayexpress
Project description:We hypothesize that under homeostatic as well as inflammatory conditions circulating monocytes and/or their bone marrow-derived progenitors might contribute to the replenishment of CD103+ and CD103- DC in lymphoid and non-lymphoid compartments. To that end, bone marrow cells from CX3CR1+/gfp C57BL/6 mice were sorted as follows: lineage negative (CD3, CD19, NK1.1, Ter119, Ly6G and CD11c) CX3CR1+c-kit+. Sorted cells were further cultured in vitro under the continuous presence of GM-CSF. lin-CX3CR1+c-kit+ bone marrow cells gave rise to CD103+ and CD103- DC in vitro. To test whether CD103 might be a suitable marker that allows the differentiation of functionally distinct DC subsets generated in vitro, CD11c+CD103+ and CD11c+CD103- DC were sorted from day 5 cultures of lin-CX3CR1+c-kit+ cells and analyzed by whole mouse genome microarrays from Agilent technologies. Compared to CD103+ DC, CD103- DC displayed a strong up-regulation of transcripts for genes involved in innate immunity, whereas those involved in costimulation were down-modulated. Our data suggest distinct functional activity of these two DC subsets. Keywords: Transcriptional profiling-Cell type comparison
2008-12-17 | GSE10882 | GEO
Project description:Abstract Two major dendritic cell (DC) subsets have been described in the islets of mice: The immunogenic CD8α-CD11b+ DCs and the tolerogenic CD8α+CD103+ DCs. We have recently reported on reduced numbers of the minor population of tolerogenic CD8α+CD103+ DCs in the pancreas of 5 week old pre-diabetic non-obese diabetic (NOD) mice. Aim: To analyze also the larger subset of CD11c+CD8α- DCs isolated from the pancreas of pre-diabetic NOD mice 1) for maturation and tolerance inducing molecules found abnormally expressed on CD8α+CD103+ DCs, and 2) for genome-wide gene expression to further elucidate abnormalities in underlying gene expression networks. Methods: CD11c+CD8α- DCs were isolated from 5 week old C57BL/6 and NOD pancreas. Expression of cell surface markers including CD86, CCR5, CD11b, CD103, Clec9a, CD24 and CD200R3 were measured by FACS. Genome-wide gene expression by microarray was assessed during the steady state and after in vitro LPS stimulation. Results: The steady state pancreatic CD11c+ CD8α- DCs during the pre-diabetic stage showed: 1) A reduced expression of several gene networks important for the prime functions of the cell, such as for cell renewal, immune stimulation and immune tolerance induction, for migration and for the provision of growth factors for beta cell regeneration. This general deficiency state was corroborated by a reduced in vivo proliferation (BrdU incorporation) of the cells and the reduced expression in FACS analysis of CD86, CCR5, CD103, Clec9a, CD24 and CD200R3 on the cells. 2) A hyper reactivity of these cells to LPS correlated with an enhanced pro-inflammatory state characterized by altered expression of a number of classical pro-inflammatory factors and cytokines. Conclusion: The NOD CD11c+CD8α- DCs seem to be Janus-faced depending on the conditions: Deficient in steady state with reduced immune stimulation capabilities also for tolerance induction; over-inflammatory with a molecular profile suggesting a preferential stimulatory capacity for Th1 cells when encountering a Pathogen-Associated Molecular Pattern (PAMP) in the form of LPS. We used microarray gene expression analysis to explain the abnormal expression of several cell surface markers involved in tolerace, migration and maturation in the steady-state and to measure the effect of a PAMP such as LPS We isolated RNA from FACS sorted CD11c+CD8α- DCs in 10 pooled pancreases from pre-diabetic NOD and non-diabetic C57BL/6 mice at 5 weeks. In addition, we treated in another experiment the isolated pancreas DCs with LPS (and PBS), incubated for 18h and measured gene expression. We compared gene expression between strains NOD vs C57BL/6 under steady-state and after in-vitro LPS/PBS stimulation.
2014-07-01 | E-GEOD-45028 | biostudies-arrayexpress
Project description:RNA-seq analyses of two intestinal dendritic cell subsets, CD103+CD11b- and CD103-CD11b+, from wild type and CbfbF/F:CD11c-Cre mice.
| PRJNA539949 | ENA
Project description:Nlrp6-/- lamina propria Ly6C-hi monocytes in response to AOM/DSS have deficient TNFα production, but increased production of other pro-inflammatory cytokines as compared to WT NLRP6 is a member of the Nod-like receptor family, whose members are involved in the recognition of microbes and/or tissue injury. NLRP6 was previously demonstrated to regulate the production of IL-18 and is important for protecting mice against chemically-induced intestinal injury and colitis-associated colon cancer. However, the cellular mechanisms by which NLRP6 reduces susceptibility to colonic inflammation remain unclear. Here, we determined that NLRP6 expression is specifically upregulated in Ly6Chi inflammatory monocytes that infiltrate into the colon during dextran sulfate sodium (DSS)-induced inflammation. Adoptive transfer of WT Ly6Chi inflammatory monocytes into Nlrp6-/- mice was sufficient to protect them from mortality, significantly reducing intestinal permeability and damage. NLRP6-deficient inflammatory monocytes were specifically defective in TNFα production, which was important for reducing DSS-induced mortality and dependent on autocrine IL-18 signaling by inflammatory monocytes. Our data reveal a previously unappreciated role for NLRP6 in inflammatory monocytes, which are recruited during intestinal injury to promote barrier function and limit bacteria-driven inflammation. This study also highlights the importance of early cytokine responses, particularly NLRP6-dependent and IL-18-dependent TNFα production in preventing chronic dysregulated inflammation. Ly6Chi monocytes were sorted from lamina propria of WT or Nlrp6-/- mice at day 10 of AOM/2%DSS. RNA was extracted and hybridized to the mouse 2.1 ST array.
2016-03-27 | E-GEOD-79631 | biostudies-arrayexpress
Project description:Abstract Two major dendritic cell (DC) subsets have been described in the islets of mice: The immunogenic CD8α-CD11b+ DCs and the tolerogenic CD8α+CD103+ DCs. We have recently reported on reduced numbers of the minor population of tolerogenic CD8α+CD103+ DCs in the pancreas of 5 week old pre-diabetic non-obese diabetic (NOD) mice. Aim: To analyze also the larger subset of CD11c+CD8α- DCs isolated from the pancreas of pre-diabetic NOD mice 1) for maturation and tolerance inducing molecules found abnormally expressed on CD8α+CD103+ DCs, and 2) for genome-wide gene expression to further elucidate abnormalities in underlying gene expression networks. Methods: CD11c+CD8α- DCs were isolated from 5 week old C57BL/6 and NOD pancreas. Expression of cell surface markers including CD86, CCR5, CD11b, CD103, Clec9a, CD24 and CD200R3 were measured by FACS. Genome-wide gene expression by microarray was assessed during the steady state and after in vitro LPS stimulation. Results: The steady state pancreatic CD11c+ CD8α- DCs during the pre-diabetic stage showed: 1) A reduced expression of several gene networks important for the prime functions of the cell, such as for cell renewal, immune stimulation and immune tolerance induction, for migration and for the provision of growth factors for beta cell regeneration. This general deficiency state was corroborated by a reduced in vivo proliferation (BrdU incorporation) of the cells and the reduced expression in FACS analysis of CD86, CCR5, CD103, Clec9a, CD24 and CD200R3 on the cells. 2) A hyper reactivity of these cells to LPS correlated with an enhanced pro-inflammatory state characterized by altered expression of a number of classical pro-inflammatory factors and cytokines. Conclusion: The NOD CD11c+CD8α- DCs seem to be Janus-faced depending on the conditions: Deficient in steady state with reduced immune stimulation capabilities also for tolerance induction; over-inflammatory with a molecular profile suggesting a preferential stimulatory capacity for Th1 cells when encountering a Pathogen-Associated Molecular Pattern (PAMP) in the form of LPS. We used microarray gene expression analysis to explain the abnormal expression of several cell surface markers involved in tolerace, migration and maturation in the steady-state and to measure the effect of a PAMP such as LPS
2014-07-01 | GSE45028 | GEO
Project description:CD103+CD11b+ dendritic cells (DC) are unique to the intestine, but the factors governing their differentiation are unclear. Here we show that transforming growth factor receptor 1 (TGF beta 1) has an indispensable, cell intrinsic role in the development of these cells. Deletion of Tgfbr1 results in markedly fewer intestinal CD103+CD11b+ DCs and a reciprocal increase in the CD103–CD11b+ DC subset. Transcriptional profiling identifies markers that define the CD103+CD11b+ DC lineage, including CD101, TREM1 and Siglec-F, and shows that the absence of CD103+CD11b+ DCs in CD11c-Cre.Tgfbr1fl/fl mice reflects defective differentiation from CD103–CD11b+ intermediaries, rather than an isolated loss of CD103 expression. The defect in CD103+CD11b+ DCs is accompanied by reduced generation of antigen-specific, inducible FoxP3+ regulatory T (Treg) cells in vitro and in vivo, and by reduced numbers of endogenous TH17 cells in the intestinal mucosa. Thus, TGF beta 1 mediated signalling may explain the tissue-specific development of these unique DCs.
2017-06-23 | GSE100393 | GEO
Project description:We report phenotypes in gut dendritic cell development by loss of Runx/Cbfb transcription factor complexes. To further examine function of residual CD103+CD11b- and CD103-CD11b+ DCs, we performed RNA-seq analyses and compared gene expression signatures between control and Cbfb-deficient cells.
2019-08-01 | GSE130380 | GEO