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Identifcation of Human B1 cells

ABSTRACT: The mission of B lymphocytes is considered to reside primarily in immunoglobulin production; however, the success of B cell depletion in autoimmune diseases previously thought to be T cell-mediated suggests that some B cells fulfill other roles in autoimmunity. We examined the recently identified human B1 cell population for T cell stimulatory activity. We found two kinds of B1 cells that are distinguished by multiple surface markers and distinct transcriptomic profiles. In both umbilical cord and adult peripheral blood, the larger of the two, which is CD11b-, constitutes about 90% of B1 cells, whereas the smaller of the two, which is CD11b+, constitutes about 10% of B1 cells. These B1 cell populations differ functionally. CD11b- B1 cells spontaneously secrete much more IgM than CD11b+ B1 cells. In contrast, CD11b+ B1 cells express more CD86, and efficiently stimulate more T cell expansion, than CD11b- B1 cells. These CD11b+ B1 cells are markedly elevated in lupus patients and express increased CD86 and increased T cell stimulating activity in disease. This work distinguishes a novel, T cell-interacting B1 cell population whose expression and activity may be a reflection of, and a therapeutic target in, autoimmune disease. abstract

ORGANISM(S): Homo sapiens

PROVIDER: GSE29717 | GEO | 2011/11/08

SECONDARY ACCESSION(S): PRJNA141091

REPOSITORIES: GEO

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Identifcation of Human B1 cells

Project description:The mission of B lymphocytes is considered to reside primarily in immunoglobulin production; however, the success of B cell depletion in autoimmune diseases previously thought to be T cell-mediated suggests that some B cells fulfill other roles in autoimmunity. We examined the recently identified human B1 cell population for T cell stimulatory activity. We found two kinds of B1 cells that are distinguished by multiple surface markers and distinct transcriptomic profiles. In both umbilical cord and adult peripheral blood, the larger of the two, which is CD11b-, constitutes about 90% of B1 cells, whereas the smaller of the two, which is CD11b+, constitutes about 10% of B1 cells. These B1 cell populations differ functionally. CD11b- B1 cells spontaneously secrete much more IgM than CD11b+ B1 cells. In contrast, CD11b+ B1 cells express more CD86, and efficiently stimulate more T cell expansion, than CD11b- B1 cells. These CD11b+ B1 cells are markedly elevated in lupus patients and express increased CD86 and increased T cell stimulating activity in disease. This work distinguishes a novel, T cell-interacting B1 cell population whose expression and activity may be a reflection of, and a therapeutic target in, autoimmune disease. abstract Four groups each group comprising 3 samples for a total of 12 samples of human B cells were analyzed

2011-11-08 | E-GEOD-29717 | biostudies-arrayexpress

LKB1 expressed in dendritic cells governs the development and expansion of thymus-derived regulatory T cells

Project description:Liver Kinase B1 (LKB1) plays a key role in cellular metabolism by controlling AMPK activation. However, its function in dendritic cell (DC) biology has not been addressed. Here, we find that LKB1 functions as a critical brake on DC immunogenicity, and when lost, leads to reduced mitochondrial fitness and increased maturation, migration, and T cell priming of peripheral DCs. Concurrently, loss of LKB1 in DCs enhances their capacity to promote output of regulatory T cells (Tregs) from the thymus, which dominates the outcome of peripheral immune responses, as suggested by increased resistance to asthma and higher susceptibility to cancer in CD11cΔLKB1 mice. Mechanistically, we find that loss of LKB1 specifically primes thymic CD11b+ DCs to facilitate thymic Treg development and expansion, which is independent from AMPK signalling, but dependent on mTOR and enhanced phospholipase C β1-driven CD86 expression. Together, our results identify LKB1 as a critical regulator of DC-driven effector T cell and Treg responses both in the periphery and the thymus.

2020-05-07 | GSE149941 | GEO

Loss of lamin B1 results in prolongation of S-phase and decondensation of chromosome territories in the interphase nucleus of mammalian cells

Project description:Nuclear lamin B1 constitutes one of the major structural proteins in the lamina mesh. We silenced the expression of lamin B1 by RNA interference in the colon cancer cell line DLD-1 and showed a dramatic redistribution of H3K27me3 from the periphery to a more homogeneous nuclear dispersion; in addition we observed an increased frequency of micronuclei and nuclear blebs. By 3D-FISH analyses, we demonstrate that the volume and surface of chromosome territories were significantly larger in LMNB1-depleted cells, suggesting that lamin B1 is required to maintain chromatin condensation in interphase nuclei. These changes led to a prolonged S-phase due to activation of Chk1 and telomere attrition. Finally, silencing of LMNB1 resulted in extensive changes in alternative splicing of multiple genes and in a higher number of enlarged nuclear speckles. Taken together, our results suggest a mechanistic role of the nuclear lamina in the organization of chromosome territories, maintenance of genome integrity and proper gene splicing. This dataset includes the comparison of gene transcripts between cells with silenced lamin B1 and empty vector negative control transfected cells.

2014-07-16 | GSE53546 | GEO

Microarray analysis of CX3CR1high CD11b+ CD11c+ cells in murine intestinal lamina propria

Project description:Several innate immune cell subsets have recently been identified to maintain gut homeostasis in both human and mice. Among these subsets, CX3CR1high CD11b+ CD11c+ cells contribute to intestinal tolerance through various mechanisms in mice. However, whether tolerogenic innate myeloid cells are present in the human intestine is not clearly defined. In this manuscript, we identified an intestinal myeloid cell subset possessing tolerogenic ability. HLA-DRhigh CD14+ CD163high cells in the human colon were divided into two subsets based on CD160 expression: CD163high CD160high and CD163high CD160low cells. Both cell subsets exhibited high levels of IL-10 production and high phagocytic activities. CD163high CD160high cells suppressed effector CD4+ T cell proliferation by a Foxp3+ Treg cell induction-independent mechanism. We further observed that the number and suppressive activity of these cells were profoundly decreased in patients with ulcerative colitis (UC). In addition, CD163high CD160high cells in the UC patients showed inflammatory phenotype, such as increased expression of IL6, CD80, and CD86, accompanied with decreased IL10RB expression. Our results highlight that a tolerogenic CD163high CD160high cell subset might be implicated in the prevention of UC development. Gene expression analysis of murine CX3CR1high cells (n=10) and murine blood Ly6c+ CD11b+ monocytes (n=6) were performed using Whole Mouse Genome Microarray Kit, 4x44K V2 (G4846A) as dye-swapped experiments.

2016-07-17 | E-GEOD-79628 | biostudies-arrayexpress

Loss of lamin B1 results in prolongation of S-phase and decondensation of chromosome territories in the interphase nucleus of mammalian cells

2014-07-16 | E-GEOD-53546 | biostudies-arrayexpress

Isolation of human skeletal muscle precursor cells by fluorescence-activated cell sorting.

Project description:Novel fluorescence-activated cell sorting (FACS) strategies to prospectively purify functionally distinct cell populations from the human myofiber-associated (hMFA) cell compartment, including human Skeletal Muscle Precursor cells (hSMPs): HSMPs, identified as CD45-Mac1-GlyA-CD31-CD34-CD56intITGA7hi hMFA cells, are highly enriched for cells expressing the satellite cell marker PAX7 and show efficient myogenic and lack adipogenic capacity. CD45-CD11b-GlyA-CD31-CD34+ hMFA cells (CD34+ cells) do not express PAX7, lack myogenic and exhibit adipogenic activity.

2014-01-08 | GSE44227 | GEO

Isolation of human skeletal muscle precursor cells by fluorescence-activated cell sorting.

2014-01-08 | E-GEOD-44227 | biostudies-arrayexpress

Transcription profiling of mouse splenic B cells expressing a dominant-negative p300 allele which lacks histone acetyltransferase activity

Project description:The p300 protein is one of more than 15 known mammalian HATs. We have used mice that carry a mutant allele of the p300 gene, which encodes a full-length protein that, however, lacks detectable acetyltransferase (AT)-activity and that acts in a dominant-negative manner. In addition, the allele is conditional, so that it can be expressed in a tissue-specific manner with the help of mice that express Cre-recombinase. Expression of the mutant allele specifically in B-cells, using CD19-cre mice, results in premature death with full penetrance from an autoimmune disease that closely mimics systemic lupus erythematosus (SLE) in its pathological manifestations.

2006-07-01 | E-MEXP-747 | biostudies-arrayexpress

Defining the microglia transcriptome during disease progression in ALS transgenic mice

Project description:Purpose: We purified spinal cord microglia utilizing percoll gradients and magnetic beads, followed by transcriptome profiling (RNA-seq) to define microglia expression profiles against other neural, immune cell-types. We next observed how the microglial transcriptomes change during activation in the SOD1-G93A mouse model of motor neuron degeneration at 3 time points. We also compared these profiles with that induced by LPS injection. Results and conclusions: ALS microglia were found to differ substantially from those activated by LPS and from M1/M2 macrophages by comparison with published datasets. These ALS microglia showing substantial induction of a neurodegeneration-tailored phenotype, with induction of lysosomal, RNA splicing, and Alzheimer's disease pathway genes. Overall they express a mixture of neuroprotective and neurotoxic factors during activation in ALS mice, showing that neuro-immune activation in the spinal cord is a double-edged sword. We also detected the transcriptional nature of surface marker expression in microglia (CD11b, CD86, CD11c), and substantial T-cell microglia cross-talk using correlative microglia transcriptome/FACS analysis. 42 total RNA samples from purified spinal cord microglia were subjected to paired-end RNA-sequencing. Parallel flow cytometry data was collected from the same spinal cords.

2013-07-15 | E-GEOD-43366 | biostudies-arrayexpress

Microarray analysis of CD14+ CD163high CD160high cells in human intestinal lamina propria

Project description:Several innate immune cell subsets have recently been identified to maintain gut homeostasis in both human and mice. Among these subsets, CX3CR1high CD11b+ CD11c+ cells contribute to intestinal tolerance through various mechanisms in mice. However, whether tolerogenic innate myeloid cells are present in the human intestine is not clearly defined. In this manuscript, we identified an intestinal myeloid cell subset possessing tolerogenic ability. HLA-DRhigh CD14+ CD163high cells in the human colon were divided into two subsets based on CD160 expression: CD163high CD160high and CD163high CD160low cells. Both cell subsets exhibited high levels of IL-10 production and high phagocytic activities. CD163high CD160high cells suppressed effector CD4+ T cell proliferation by a Foxp3+ Treg cell induction-independent mechanism. We further observed that the number and suppressive activity of these cells were profoundly decreased in patients with ulcerative colitis (UC). In addition, CD163high CD160high cells in the UC patients showed inflammatory phenotype, such as increased expression of IL6, CD80, and CD86, accompanied with decreased IL10RB expression. Our results highlight that a tolerogenic CD163high CD160high cell subset might be implicated in the prevention of UC development. Gene expression analysis of pooled lamina propria cells (LPCs) (n=12) and human blood CD14+ monocytes (n=7) were performed using Whole Human Genome Microarray Kit, 4x44K (G4112F) as one-color experiments.

2016-07-17 | E-GEOD-79627 | biostudies-arrayexpress

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