ILC3 contain 3 well-defined subsets, CCR6+ ILC3, NKp46+ ILC3, and CCR6NKp46 DN ILC3. These subsets had not previously been transcriptionally compared and the extent to which they had shared or unique transcriptional profiles remained unclear.
IL-15 sustains IL-7R-independent ILC2 and ILC3 development.
Specimen part
View SamplesWe examined the role of TREM2 on microglia responses to demyelination
TREM2 sustains microglial expansion during aging and response to demyelination.
Sex, Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Distinct Gene Regulatory Pathways for Human Innate versus Adaptive Lymphoid Cells.
Specimen part
View SamplesInnate lymphoid cells (ILCs) serve as sentinels in mucosal tissues, sensing release of soluble inflammatory mediators, rapidly communicating danger via cytokine secretion, and functioning as guardians of tissue homeostasis. Although ILCs have been studied extensively in model organisms, little is known about these first responders in humans, especially their lineage and functional kinships to cytokine-secreting T helper cell (Th) counterparts. Here, we report gene regulatory circuitries for four human ILCTh counterparts derived from mucosal environments, revealing that each ILC subset diverges as a distinct lineage from Th and circulating natural killer cells, but shares circuitry devoted to functional polarization with their Th counterparts. Super-enhancers demarcate cohorts of cell identity genes in each lineage, uncovering new modes of regulation for signature cytokines, novel molecules that likely impart important functions to ILCs, and potential mechanisms for autoimmune disease SNP associations within ILCTh subsets.
Distinct Gene Regulatory Pathways for Human Innate versus Adaptive Lymphoid Cells.
Specimen part
View SamplesThe subsets of immune cells within the human placenta are incompletely described. We used microarray to determine the transcriptional differences between two myeloid subsets in the term human placenta.
Two Distinct Myeloid Subsets at the Term Human Fetal-Maternal Interface.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling.
Specimen part
View SamplesAmong the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection.
SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling.
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View SamplesAmong the features that distinguish type 1 innate lymphoid cells (ILC1s) from NK cells is a gene signature indicative of TGFb-family cytokine imprinting. To assess the impact of TGFb family cytokines on ILC1 differentation, we examined SMAD4- a transcription factor that facilitates the signaling pathway common to all TGFb family cytokines-was specifically ablated in ILCs and NK cells. While SMAD4 deficiency did not affect ILC1 differentation, NK cells paradoxically aquired an ILC1-like gene signature and were incapable of controlling tumor metastasis and viral infection.
SMAD4 impedes the conversion of NK cells into ILC1-like cells by curtailing non-canonical TGF-β signaling.
Specimen part
View SamplesRNA was isolated from FFPE samples of IDH1 mutant, WT tumors and normal brains Overall design: Determination of the glioma subtype in IDH1 mutant and WT tumors
Mutant IDH1 Promotes Glioma Formation In Vivo.
Specimen part, Subject
View SamplesWe examined the role of TREM2 on microglia responses to amyloid-beta deposition in a mouse model of Alzheimer's disease
TREM2 lipid sensing sustains the microglial response in an Alzheimer's disease model.
Age, Specimen part
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