To delineate the mechanism by which human mitochondrial transcriptional factor A (hTFAM) suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment.
Human mitochondrial transcriptional factor A breaks the mitochondria-mediated vicious cycle in Alzheimer's disease.
Specimen part
View SamplesTo delineate the mechanism by which hTFAM suppresses AD pathology in the neuron model of AD, we first performed microarray analyses using using RNAs prepared from PS1P117L and wild-type neurons. Next, we performed microarray analyses using PS1P117L neurons with or without recombinant hTFAM protein treatment.
Human mitochondrial transcriptional factor A breaks the mitochondria-mediated vicious cycle in Alzheimer's disease.
Specimen part, Treatment
View SamplesTo delineate the mechanism underlying the amelioration of AD pathophysiology by hTFAM, we performed gene expression profiling using hippocampal RNAs from the AD model mouse and AD model mouse overexpressing human TFAM.
Human mitochondrial transcriptional factor A breaks the mitochondria-mediated vicious cycle in Alzheimer's disease.
Sex, Age, Specimen part
View SamplesTo identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD)
Altered expression of diabetes-related genes in Alzheimer's disease brains: the Hisayama study.
Sex, Age, Specimen part
View SamplesTo identify molecular pathological alterations in AD brains, we performed interspecies comparative microarray analyses using RNAs prepared from postmortem human brain tissues donated for the Hisayama study and hippocampal RNAs from the triple-transgenic mouse model of AD (3xTg-AD)
Altered expression of diabetes-related genes in Alzheimer's disease brains: the Hisayama study.
Sex, Age, Specimen part
View SamplesIgE plays an essential role in the pathogenesis of allergies and its production is strongly regulated. A transient IgE germinal center phase and lack of IgE memory cells limit the generation of pathogenic IgE, but this can be overcome by sequential switching of IgG1 cells to IgE. We investigated which population of IgG1 cells can give rise to IgE-producing cells in memory responses. We identified three populations of IgG1 memory B cells (DP:CD73+CD80+, SP:CD73-CD80+, DN:CD73-CD80-) that generate IgE plasma cells of high or low affinity, but none gives rise to IgE germinal center cells or IgE memory cells. The two memory IgG1 populations differ however in their ability to differentiate into IgG1 plasma cells and germinal center cells, and to expand the IgG1 memory B cell pool. To explore the molecular mechanisms that may explain the distinct functions of IgG1 memory B cell subsets we compared their expression by transcriptome analysis using next generation sequencing. Overall design: mRNA profiles of quadruplicates of double positive (DP:CD73+CD80+), single positive (SP:CD73-CD80+), double negative (DN:CD73-CD80-) IgG1 memory B cells along with IgG1 germinal center (GC) cells and naïve B cells were generated using Illumina high throughput sequencing.
IgG1 memory B cells keep the memory of IgE responses.
Specimen part, Cell line, Subject
View SamplesThe mechanisms involved in the maintenance of memory IgE responses are poorly understood, and the role played by germinal center (GC) IgE cells in these memory responses is particularly unclear. IgE B-cell differentiation is characterized by a transient GC phase, a bias towards the plasma cell (PC) fate, and dependence on sequential switching for the production of high-affinity IgE. We show here that IgE GC B cells are unfit to undergo the conventional GC differentiation program due to impaired B-cell receptor function and increased apoptosis. IgE GC cells fail to populate the GC light zone and are unable to contribute to the memory and long-lived PC compartments. Furthermore, we demonstrate that direct and sequential switching are linked to distinct B-cell differentiation fates: direct switching generates IgE GC cells, whereas sequential switching gives rise to IgE plasma cells. We propose a comprehensive model for the generation and memory of IgE responses.
The distinctive germinal center phase of IgE+ B lymphocytes limits their contribution to the classical memory response.
Specimen part, Treatment
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Neuropilin 1 is expressed on thymus-derived natural regulatory T cells, but not mucosa-generated induced Foxp3+ T reg cells.
Specimen part
View SamplesiTreg cells from Tbmc mLN mice treated with one week of 1% Oral Ova were compared to Total Treg from WT mice.
Neuropilin 1 is expressed on thymus-derived natural regulatory T cells, but not mucosa-generated induced Foxp3+ T reg cells.
Specimen part
View SamplesTo compare subpopulations of Treg cells in wild type mice based upon Nrp1 Expression, differentiating nTreg and iTreg
Neuropilin 1 is expressed on thymus-derived natural regulatory T cells, but not mucosa-generated induced Foxp3+ T reg cells.
Specimen part
View Samples