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accession-icon GSE29806
Naturally transmitted segmented filamentous bacteria segregate with diabetes protection in NOD mice
  • organism-icon Mus musculus
  • sample-icon 26 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Vertebrates typically harbor a rich gastrointestinal microbiota, which has co-evolved with the host over millennia and is essential for several of its physiological functions, in particular maturation of the immune system. Recent studies have highlighted the importance of a single bacterial species, segmented filamentous bacteria (SFB), in inducing a robust T helper (Th)17 population in the small intestinal lamina propria (SI-LP) of the mouse gut. Consequently, SFB can promote IL-17-dependent immune and autoimmune responses, gut-associated as well as systemic, including inflammatory arthritis and experimental autoimmune encephalomyelitis. Here, we exploit the incomplete penetrance of SFB colonization of NOD mice in our animal facility to explore its impact on the incidence and course of type-1 diabetes in this prototypical, spontaneous model. There was a strong co-segregation of SFB-positivity and diabetes protection in females, but not in males, which remained relatively disease-free regardless of the SFB status. In contrast, insulitis did not depend on SFB colonization. SFB-positive, but not SFB-negative, females had a substantial population of Th17 cells in the SI-LP, which was the only significant, repeatable difference in the examined T cell compartments of the gut, pancreas or systemic lymphoid tissues. Th17 signature transcripts dominated the very limited SFB-induced molecular changes detected in SI-LP CD4+ T cells. Thus, a single bacterium, and the gut immune system alterations associated with it, can either promote or protect from autoimmunity in predisposed mouse models, likely reflecting their variable dependence on different Th subsets.

Publication Title

Naturally transmitted segmented filamentous bacteria segregate with diabetes protection in nonobese diabetic mice.

Sample Metadata Fields

Age, Specimen part

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accession-icon GSE71343
Control of Peripheral Tolerance by Regulatory T Cell-Intrinsic Notch Signaling
  • organism-icon Mus musculus
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Notch receptors direct the differentiation of T helper (Th) cell subsets, but their influence on regulatory T (TR) cell responses is obscure. Interruption of Notch signaling in TR cells resulted in a super-regulatory phenotype, with suppression of TR cell Th1 programming and apoptosis as well as Th1 cell responses in systemic inflammation. In contrast, gain of function Notch1 signaling in TR cells resulted in lymphoproliferation, dysregulated Th1 responses and autoimmunity. To determine mechanisms by which Notch signaling may alter TR cell function, we compared the transcriptional profiles of splenic TR cells of Foxp3EGFPCre mice with those of Foxp3EGFPCreR26N1c/N1c (gain of function Notch signaling), Foxp3EGFPCreRBPJ/ (loss of function canonical Notch signaling), and Foxp3EGFPCreR26N1c/N1cRBPJ/ mice (gain of function/canonical loss of function Notch signaling).

Publication Title

Control of peripheral tolerance by regulatory T cell-intrinsic Notch signaling.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE50098
A special population of regulatory T cells potentiates muscle regeneration
  • organism-icon Mus musculus
  • sample-icon 63 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

A special population of regulatory T cells potentiates muscle repair.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment, Time

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accession-icon GSE50096
Regulatory T cells from injured skeletal muscle
  • organism-icon Mus musculus
  • sample-icon 24 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A phenotypically and functionally distinct population of CD4+ Foxp3+ T cells (Tregs) rapidly accumulates in acutely injured skeletal muscle of mice, just as invading myeloid-lineage cells switch from a pro-inflammatory to a pro-regenerative state. Analysis of gene expression of Tregs and CD4+Foxp3- T cells (Tconvs) from injured muscle and spleen revealed that the transcriptome of muscle Treg cells is distinct from that of splenic Tregs. A set of genes is uniquely expressed by muscle Tregs, while another set is over-expressed by the two muscle populations vis--vis their two spleen counterparts.

Publication Title

A special population of regulatory T cells potentiates muscle repair.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment, Time

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accession-icon GSE50094
Gene expression profiling of injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).
  • organism-icon Mus musculus
  • sample-icon 21 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

A comparative analysis of gene expression of injured skeletal muscle from wild-type (Foxp3-DTR-) and Treg-depleted (Foxp3-DTR+) mice showed that Treg cells are critical for effective repair and regeneration of acute injury of skeletal muscle.

Publication Title

A special population of regulatory T cells potentiates muscle repair.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment, Time

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accession-icon GSE50097
Effect of Amphiregulin on global gene expression in injured skeletal muscle in the presence or absence of CD4+Foxp3+ regulatory T cells (Tregs).
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Global gene expression analysis of injured skeletal muscle showed that amphiregulin (Areg), a growth factor over-expressed by muscle Treg cells, enhances muscle regeneration both in the presence and in the absence of Tregs.

Publication Title

A special population of regulatory T cells potentiates muscle repair.

Sample Metadata Fields

Age, Specimen part, Treatment, Time

View Samples
accession-icon GSE50095
Effects of Treg depletion in dystrophic muscle.
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

CD4+Foxp3+ regulatory T cells (Tregs) accumulate in skeletal muscle from dystrophin-deficient mdx mice. Analysis of global gene expression in muscles from mdx mice treated with anti-CD25 compared with muscles from mdx mice treated with control antibody revealed that Tregs partially protect mdx mice from muscle pathology and promote muscle repair/regeneration.

Publication Title

A special population of regulatory T cells potentiates muscle repair.

Sample Metadata Fields

Sex, Age, Specimen part, Treatment

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accession-icon GSE88919
Mining the microbiome for modulatory effects on the murine intestinal transcriptome
  • organism-icon Mus musculus
  • sample-icon 148 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Within the human gut reside diverse microbes coexisting with the host in a mutually advantageous relationship. We comprehensively identified the modulatory effects of phylogenetically diverse human gut microbes on the murine intestinal transcriptome. Gene-expression profiles were generated from the whole-tissue intestinal RNA of mice colonized with various single microbial strains. The selection of microbe-specific effects, from the transcriptional response, yielded only a small number of transcripts, indicating that symbiotic microbes have only limited effects on the gut transcriptome overall. Moreover, none of these microbe-specific transcripts was uniformly induced by all microbes. Interestingly, these responsive transcripts were induced by some microbes but repressed by others, suggesting different microbes can have diametrically opposed consequences.

Publication Title

Mining the Human Gut Microbiota for Immunomodulatory Organisms.

Sample Metadata Fields

Sex, Age, Specimen part

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accession-icon GSE87678
Transcriptional response of small intestinal epithelial cells (S-IECs) to bacterial monocolonization
  • organism-icon Mus musculus
  • sample-icon 13 Downloadable Samples
  • Technology Badge Icon Affymetrix Mouse Gene 1.0 ST Array (mogene10st)

Description

Here we analyzed the transcriptional profile of S-IECs sorted from GF and monocolonized mice (C. histolyticum and B. adolescentis), as well as SPF mice colonized with SFB or not.

Publication Title

Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice.

Sample Metadata Fields

Sex, Age

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accession-icon SRP092209
Transcriptional response of small-intestinal lamina propria CD4+ T cells to bacterial colonization
  • organism-icon Mus musculus
  • sample-icon 12 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

We analyzed the transcriptional profile of small-intestinal lamina propria (SI-LP) CD4+ T cells isolated from germ-free and mice monocolonized with Bifidobacterium adolescentis, SFB, and Nexabiotic (a 23-strain, Th17-inducing, probiotic mix). Overall design: CD4+ T cells were double-sorted from mice directly into lysis buffer.

Publication Title

Identifying species of symbiont bacteria from the human gut that, alone, can induce intestinal Th17 cells in mice.

Sample Metadata Fields

Sex, Age, Specimen part, Cell line, Subject

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refine.bio is a repository of uniformly processed and normalized, ready-to-use transcriptome data from publicly available sources. refine.bio is a project of the Childhood Cancer Data Lab (CCDL)

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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