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Gene expression profile of Age associated B cells, Follicular B cells, and B1 cells

ABSTRACT: We performed gene expression profile of different B cell populations found in old (18 months old) C57BL/6 female mouse (B1 cells were recovered from both young and old C57BL/6 mice). Mice were naïve and healthy (no autoimmunity was detected at the time of the experiment). Different B cell populations were sorted using flow cytometry and RNA was isolated.

ORGANISM(S): Mus musculus

SUBMITTER: Anatoly Rubtsov

PROVIDER: E-GEOD-28887 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Toll-like receptor 7 (TLR7)-driven accumulation of a novel CD11c⁺ B-cell population is important for the development of autoimmunity.

Rubtsov Anatoly V AV Rubtsova Kira K Fischer Aryeh A Meehan Richard T RT Gillis Joann Z JZ Kappler John W JW Marrack Philippa P

Blood 20110504 5

Females are more susceptible than males to many autoimmune diseases. The processes causing this phenomenon are incompletely understood. Here, we demonstrate that aged female mice acquire a previously uncharacterized population of B cells that we call age-associated B cells (ABCs) and that these cells express integrin α(X) chain (CD11c). This unexpected population also appears in young lupus-prone mice. On stimulation, CD11c(+) B cells, both from autoimmune-prone and healthy strains of mice, secr ...[more]

PMID: 21543762

Similar Datasets

Gene expression profile of Age associated B cells, Follicular B cells, and B1 cells

Project description:We performed gene expression profile of different B cell populations found in old (18 months old) C57BL/6 female mouse (B1 cells were recovered from both young and old C57BL/6 mice). Mice were naïve and healthy (no autoimmunity was detected at the time of the experiment).

2011-04-28 | GSE28887 | GEO

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

Analysis of proposed human B1 cells

Project description:The recent discovery of the human B1 cells, identified by the expression of CD20, CD27 and CD43 in absence of expression of CD70 and CD69 has been subject of debate. Some studies have raised the possibility that these cells are B cells differentiating towards the plasmablast and plasma cell stage rather than being the human counterpart of murine B1 cells. No further in depth studies have been performed. Therefore, a functional comparison was made between, the proposed B1 cells and plasmablasts. We observed that for several functional characteristics (distribution of isotypes of spontaneously producted antibodies, production of antigen-specific antibodies after vaccination with both T-cell dependent as well as T-cell independent antigen, the proposed B1 cells behaved similar to plasmablasts. In addition, we were able to differentiate the proposed B1 cells in vitro, indicating that they are not from a distinct lineage as the murine B1 cells. Gene expression analysis revealed that these cells cluster between memory B cells and plasmablasts, contradicting them being the genuine human counterpart of murine B1 cells, rather revealing a preplasmablast phenotype. Different B cells subsets were isolated from PBMC from healthy donors by a combination of magnetic and fluorescence activated cell sorting

2013-05-01 | E-GEOD-42724 | biostudies-arrayexpress

miRNA expression between CD4+PD1+ and CD4+PD1- T cells

Project description:Recent success in cancer immunotherapy has come from the blockade of inhibitory receptors on T cells, such as programmed cell death-1, which can induce a state of T cell exhaustion upon constant antigen stimulation. Understanding miRNA regulation of PD1 can be useful to discover miRNAs for use in therapy or as prognostic markers in various diseases including cancer, autoimmunity and transplantation. We used microarrays to discover global miRNA expression changes upon PD1 upregulation and identified miRNAs that are both up- and down-regulated. B16F10 cells were injected subcutaneously into C57BL/6 mice and 16 days later CD4+PD1+ and CD4+PD1- were sorted from the lymph nodes and spleen for RNA extraction and hybridization on Affymetrix miRNA array.

2015-08-01 | E-GEOD-65208 | biostudies-arrayexpress

Identifcation of Human B1 cells

2011-11-08 | GSE29717 | GEO

Cells with Surface Expression of CD133highCD71low are Enriched for Colony-Forming Progenitor Cells in the Adult Murine Pancreas

Project description:Previously, we identified tripotent colony-forming progenitor cells in the adult murine pancreas that were capable of self-renewal and differentiation into duct, acinar and endocrine cells in vitro. However, the incidence of these progenitor cells was low (~1% among pancreatic cells in adult 2-4 month-old mice). The goal of the current study was to find cell-surface markers that can distinguish and enrich pancreatic colony-forming progenitor cells. It was found that pancreatic cells could be divided into CD133+CD71- , CD133highCD71low and CD133lowCD71low and CD133-CD71- cells. CD133highCD71low cells, but not other cell populations, were the most enriched for colony-forming progenitors. Interestingly, both CD133+CD71- and CD133highCD71low cells expressed ductal markers as shown by gene expression RT-PCR analysis. To further characterize CD133+CD71- (designated as R1 cells) and CD133highCD71low (designated as R2 cells) ductal cell populations, genome-wide gene expression analysis using RNA-seq was performed. The genes that were differentially expressed by R1 and R2 cells are deposited here. Subsequent pathway analysis of the RNA-seq data revealed that R2 and R1 cells have propensity for cell migration and immune response, respectively. These gene expression analyses suggested ductal cells of the adult pancreas are heterogeneous in nature. Two populations of cells are sorted from the pancreas of adult 2-4 month old C57Bl/6 mice and their RNA profiles are determined. These cell populations are CD133(high)CD71(low) cells (3 samples) and CD133(positive)CD71(negative) (2 samples).

2016-07-03 | E-GEOD-72990 | biostudies-arrayexpress

Expression data from Ctla4-/- and DKO CD4+ Tconv cells

Project description:Ctla4-/- mice suffer from a severe autoimmunity characterized by indiscriminate self-reactive T cell activation. Itk-/-Ctla4-/- (DKO) mice are protected from lethal autoimmunity despite a fulminant autoimmune process in the LNs as self-reative T cells fail to migrate to destroy tissues. We used microarray to identify underlying differences in gene expression that could account for lack of migration of DKO T cells into tissues. CD4+CD25neg T cells from 3 weeks old male Ctla4-/- or DKO mice were sorted in duplicates, RNA was extracted using TRIzol reagent and microarray analysis performed with the Affymetrix MoGene 1.0 ST array

2013-09-25 | E-GEOD-51099 | biostudies-arrayexpress

Loss of Foxp3-driven epigenetic modification leads to regulatory T cell insufficiency

Project description:Regulatory T cells (Tregs) are responsible for limiting autoimmunity and chronic inflammation. Foxp3 is a transcription factor that acts as a master regulator of Treg development and function. A serendipitous observation led to the realization that a well-characterized Foxp3gfp reporter mouse, which expresses an N-terminal GFP-Foxp3 fusion protein, is a hypomorph that causes profoundly accelerated autoimmune diabetes on a NOD background. Although natural Treg development and in vitro function is not significantly altered in Foxp3gfp NOD and C57BL/6 mice, Treg fitness function in inflammatory environments is perturbed and TGF?-induced Treg development reduced. Foxp3gfpis unable to interact with the histone acetyltransferase Tip60, the histone deacetylase HDAC7, and the Ikaros family zinc finger 4, Eos, which leads to reduced Foxp3 acetylation and enhanced K48-linked polyubiquitylation. Collectively this leads to an altered transcriptional landscape and reduced Foxp3-mediated gene repression, notably at the hallmark IL-2 promoter. Loss of controlled Foxp3-driven epigenetic modification leads to Treg insufficiency that causes autoimmunity in prone environments. 16 samples overall split between 2 genotypes (wild type and Foxp3 knock in) and two cell types (Tregs and Tconv)

2012-12-07 | E-GEOD-35164 | biostudies-arrayexpress

Follicular helper T cell signature in Type 1 Diabetes

Project description:This study set out to examine CD4 T cell differentiation in a mouse model of diabetes based on transgenic expression of ovalbumin under the control of the rat insulin promoter and co-expression of the DO11.10 transgene (DO11 x rip-mOVA mice). The transcriptome of T cells isolated from the pancreatic lymph nodes (lymph nodes draining the site of self antigen expression) was compared with that of T cells isolated from inguinal lymph nodes (non-draining lymph nodes). T cells were sorted based on expression of CD4, DO11.10 TCR (KJ-126), CD25 and CD69. Primary cells from 6 week old DO11 x rip-mOVA mice were isolated ex-vivo from the pancreatic lymph nodes or inguinal lymph nodes. Cells were sorted by flow cytometry using antibodies to CD4, DO11.10 TCR (KJ-126+), CD25 and CD69. 3-6 replicates were collected per experimental group with each replicate deriving from 14 mice. RNA was isolated using the RNeasy micro kit (Qiagen).

2014-10-07 | E-GEOD-62104 | biostudies-arrayexpress

RNA-Seq of IL-2-KO follicular CD8 T cells and IL-2-KO follicular CD4 T cells

Project description:Follicular CXCR5+ PD-1+ CD8 T cells (CD8 Tfc) arise in multiple models of systemic autoimmunity yet their functional contribution to disease remains in debate. Here we define the follicular localization and functional interactions of CD8 Tfc with B cells during autoimmune disease. The absence of functional T regulatory cells in autoimmunity allows for CD8 Tfc development that then expands with lymphoproliferation. CD8 Tfc are identifiable within the lymph nodes and spleen during systemic autoimmunity, but not during tissue-restricted autoimmune disease. Autoimmune CD8 Tfc cells are polyfunctional, producing helper cytokines IL-21, IL-4, and IFNγ while maintaining cytolytic proteins CD107a, granzyme B, and TNF. During autoimmune disease, IL-2-KO CD8 T cells infiltrate the B cell follicle and germinal center, including the dark zone, to induce AID in vitro in naïve B cells via IL-4 secretion. CD8 Tfc represent a unique CD8 T cell population with a diverse effector cytokine repertoire that can contribute to pathogenic autoimmune B cell response.

2022-01-22 | GSE177911 | GEO

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