GEO 数据集

主题由标题与摘要自动归类；样本量为数据集标注之和，SuperSeries 可能与其 SubSeries 重复计算。

• BL-Hi-C, Deciphering the diversities of CTCF and CTCF-s in human embryonic stem cells
  GSE280419Homo sapiens8 个样本2026-10-31

  In this study, we performed BL-Hi-C to investigate the influence of the expression of CTCF/CTCF-s on higher-order chromatin structures.
• Chronic Inflammatory Responses in Diabetic Lung and its’ Implications for Tuberculosis Infection.
  GSE280089Mus musculus8 个样本2026-10-31

  Diabetes mellitus (DM) increases (~3.11-fold) the risk of tuberculosis (TB), leading to worse disease outcomes and higher relapse rates. scRNAseq revealed compromised adaptive and innate immunity in DM-TB mice, with decreased Th1 and M1 macrophage populations. Further analysis showed hyperinflammation in DM and dampened immune responses in DM-TB, marked by increased IL-16 signaling and reduced TNF and IFN-II responses.

  单细胞
• zebrafish retina m6A epitranscriptome
  GSE186488Danio rerio4 个样本2026-10-31

  m6A epitranscriptome of the retinas of adult zebrafish was sequenced using MeRIP-seq
• Microglia Secrete MiR-146a-5p-Containing Exosomes to Regulate Neurogenesis in Depression
  GSE185777Rattus norvegicus6 个样本2026-10-31

  Enhancing neurogenesis within the hippocampal dentate gyrus is critical for maintaining brain development and function in many neurological diseases. However, the neural mechanisms underlying neurogenesis in depression remain unclear. Here, we show that microglia transfer a microglia-enriched microRNA, miR-146a-5p, via secreting exosomes to inhibit neurogenesis in depression. Overexpression of miR-146a-5p in hippocampal dentate gyrus (DG) suppresses neurogenesis and spontaneous discharge of excitatory neurons by directly targeting Krüppel-like factor 4 (KLF4). Down-regulation of miR-146a-5p expression, ameliorates adult neurogenesis deficits in DG regions and depression-like behaviors in rats. Intriguingly, circular-RNA ANKS1B acts as a miRNA sequester for miR-146a-5p to mediate posttranscriptional regulation of KLF4 expression. Collectively, these results indicate that miR-146a-5p can function as a critical factor regulating neurogenesis under conditions of pathological processes resulting from depression and suggest that microglial exosomes generate new cross-talk channels between glial cells and neurons.
• mouse B16-F10 melanoma cells vs. Runx3 expressing B16-F10 cells
  GSE161992Mus musculus1 个样本2026-10-31

  Transcriptional profiling of the mock control mouse B16-F10 melanoma cells compares with that of the B16-F10 cells retrovirally expressing Runx3. Runx3 reduced the lung metastasis potential of the B16-F10 melanoma cells. This transcriptional profiling was used to uncover the differentially expressed genes that were regulated by Runx3.
• mouse B16-F0 melanoma cells vs. B16-F10 melanoma cells
  GSE161991Mus musculus1 个样本2026-10-31

  Transcriptional profiling of the mouse B16-F0 melanoma cells compares with that of mouse B16-F10 melanoma cells. B16-F10 melanoma cell line has very strong lung metastasis potential. B16-F10 melanoma cell line origninates from B16-F0, the later of which has very weak lung metastis potential. This transcriptional profiling was used to uncover the differentially expressed genes that may be associated with the acquirement of lung metastasis potential of B16-F10 cells.
• eCLIP-seq profiling of Flag-OTUD6B-associated RNA in HEK293T cells
  GSE352643Homo sapiens4 个样本2026-10-30

  RNA associated with Flag-OTUD6B was profiled by enhanced crosslinking and immunoprecipitation sequencing (eCLIP-seq) in human HEK293T cells. Two independent biological replicates were represented by two FLAG immunoprecipitation libraries and two corresponding size-matched input (SMInput) control libraries. This experiment and the OTUD6B-knockdown Ribo-seq experiment in MDA-MB-231 cells belong to the same research study.
• Ribosome profiling of OTUD6B knockdown and scramble-control MDA-MB-231 cells
  GSE352635Homo sapiens4 个样本2026-10-30

  Ribosome profiling was performed in human MDA-MB-231 cells with shOTUD6B-41 or a scramble-control shRNA. Two independent biological replicates were included per group, yielding four paired-end sequencing libraries. Gene-level read counts and FPKM expression values were generated. This experiment and the Flag-OTUD6B eCLIP-seq experiment in HEK293T cells belong to the same research study.

  扰动筛选
• Alcohol-induced suppression of miR-1948-3p promotes an adaptive HIF-1α response to limit hepatic steatosis
  GSE352328Mus musculus8 个样本2026-10-30

  To investigate the role of HIF-1α in alcohol-associated liver disease, we performed transcriptomic profiling on liver tissues from chronic alcohol-fed mice (AF) and mice with hepatocyte-specific Hif-1α knockdown (AF+Hif-1α KD). RNA-seq analysis revealed that Hif-1α deficiency markedly altered the hepatic transcriptional landscape and identified the disruption of the PPAR signaling pathway. Overall, this dataset provides insights into the molecular mechanisms by which HIF-1α limits hepatic steatosis during alcohol exposure.
• Effects of orexin-A on human dermal papilla cells
  GSE352146Homo sapiens6 个样本2026-10-30

  We examined effects of orexin-A on human dermal papilla cells.
• StrataChip: a microphysiological system to capture dynamic keratinocyte fate and mechanical transitions during human epidermal morphogenesis
  GSE351999Homo sapiens1 个样本2026-10-30

  Epidermal development and homeostasis require precise coordination between keratinocyte differentiation and mechanics. Still, the mechanisms integrating these processes remain poorly understood in part due to limitations of existing experimental systems. Here, we introduce StrataChip, a tractable microphysiological system that enables dynamic, multimodal interrogation of human epidermal morphogenesis. The platform integrates a media perfused dermal tissue with human epidermal keratinocytes within a microfluidic device and supports rapid epidermal stratification following establishment of an air-liquid interface. High-resolution confocal imaging and single-cell RNA-sequencing demonstrate that the StrataChip recapitulates key architectural and molecular features of human epidermis, including distinct basal, spinous, and granular layers defined by canonical differentiation markers and adhesion molecule organization. Single-cell profiling reveals transcriptionally distinct basal and spinous subpopulations, including transitional states associated with suprabasal commitment. Live 3D imaging in situ captures keratinocyte morphodynamics including basal cell delamination and asymmetric division in early stages of epidermal stratification. Altogether, StrataChip provides a robust platform that is capable of dynamic and mechanistic interrogation of how gene regulation and cell mechanical changes are coupled during epidermal morphogenesis.

  单细胞
• Heterogeneity and interaction of microglia and macrophages after retinal detachment
  GSE351957Mus musculus5 个样本2026-10-30

  This study aims to systematically investigate the evolutionary processes of microglia and macrophages during the onset and progression of retinal detachment (RD).
• Single-cell RNA sequencing of pooled orthotopic pancreatic tumors derived from PKM2-WT and PKM2-K89R cells
  GSE351631Mus musculus2 个样本2026-10-30

  We performed single-cell RNA sequencing of orthotopic pancreatic tumors established in NCG mice using pancreatic cancer cells expressing wild-type PKM2 (PKM2-WT) or the lactylation-deficient PKM2 K89R mutant (PKM2-K89R). For each group, tumor tissues from five mice were pooled before single-cell library preparation, resulting in one library per group. The dataset was used to characterize the tumor microenvironment and compare cell-type composition and cellular transcriptional states between the PKM2-WT and PKM2-K89R groups, with particular focus on fibroblast and cancer-associated fibroblast (CAF) subpopulations.

  单细胞
• Transcriptomic profiling of human nucleus pulposus cells following Mulberrin treatment
  GSE351312Homo sapiens6 个样本2026-10-30

  This study profiled the transcriptomes of human nucleus pulposus cells with or without Mulberrin treatment to identify gene expression changes associated with Mulberrin exposure. genes and exploring molecular pathways potentially involved in the cellular responses to Mulberrin treatment.
• Inactivation of Irs1 in pericentral hepatocytes promotes lipid oxidation
  GSE349448Mus musculus4 个样本2026-10-30

  Hepatic metabolic zonation enables periportal (PP) and pericentral (PC) hepatocytes to perform distinct functions in glucose and lipid metabolism. Insulin signaling is also spatially organized across the liver lobule, but the transcriptional role of insulin signaling in PC hepatocytes remains incompletely understood. To define the gene-expression programs regulated by insulin signaling in PC hepatocytes, we generated mice with inducible PC-specific deletion of insulin receptor substrate 1 (Irs1) using Cyp1a2CreER (Irs1-Cyp1a2 mice). RNA sequencing was performed to compare liver gene-expression profiles between Irs1-Cyp1a2 mice and littermate controls. This dataset provides a transcriptomic resource for identifying pathways regulated by PC IRS1 signaling and for understanding how spatial insulin signaling contributes to hepatic glucose and lipid metabolism.

  空间转录组
• GPS2 attenuates cigarette smoke-induced airway epithelial injury by attenuating mitochondrial oxidative stress
  GSE347944Homo sapiens6 个样本2026-10-30

  Cigarette smoke (CS) exposure contributes to airway epithelial injury and mitochondrial dysfunction in chronic obstructive pulmonary disease (COPD). G protein pathway suppressor 2 (GPS2) is involved in mitochondrial-nuclear communication, but its role in cigarette smoke-induced airway epithelial injury remains unclear. In this study, transcriptome sequencing was performed to investigate the molecular changes associated with GPS2 deficiency in airway epithelial cells and to explore the potential mechanisms linking GPS2 to mitochondrial dysfunction and epithelial injury. Combined with public transcriptomic data and experimental validation, our results suggest that reduced GPS2 expression is associated with alterations in energy metabolism, mitochondrial function, and redox homeostasis. These data provide a transcriptomic resource for further investigating the role of GPS2 in cigarette smoke-induced airway epithelial dysfunction.
• Early Pitx2 modulation of Fgf10 directs asymmetric lung morphology
  GSE347452Mus musculus8 个样本2026-10-30

  Both the molecular cascade establishing Left-Right asymmetric anatomy, including the transcription factor Pitx2, and the signaling pathways controlling branching morphogenesis of the lung (a Left-Right asymmetric process) have been intensively studied. However, the two have never been linked. We identify Fgf10 as a Pitx2-sensitive signal in the mesenchyme of the developing mouse lung. Pitx2 suppresses Fgf10 expression, making the right lung, which lacks Pitx2 expression, grow faster than the left during the budding stage. Modulating Fgf10 dosage in the left mesenchyme is sufficient to shift levels of epithelial proliferation and thereby alter lung budding asymmetry. Pitx2 activity during the earliest lung bud stages is sufficient to establish differences in the primary airway branches, leading to subsequent asymmetric branching patterns that eventually manifest as the left-right differences in lung morphology. Thus, Pitx2 converts left-right mesenchymal identity into organ asymmetry by quantitatively tuning Fgf10-dependent epithelial growth during early lung organogenesis.
• RNA-sequencing of brain endothelial cells from Slc1a1 endothelial cell conditional knockout mice and controls
  GSE346752Mus musculus8 个样本2026-10-30

  The goal of this study was to understand the transcriptional response of brain endothelial cells to a loss of brain endothelial Slc1a1 expression. Sample GSM10039984 (ECs, control, 3) and GSM10039987 (ECs, mutant, 4) were excluded from all published analyses because of separation from its group on principal component analysis. Final analyses used n = 3 per group. The excluded sample is included in this deposition for completeness.
• A CD4-lineage erythro-myeloid progenitor within the adult bone marrow defines an alternative pathway for macrophage generation [scRNA-Seq]
  GSE345262Mus musculus3 个样本2026-10-30

  Tissue-resident macrophages originate from distinct developmental sources, but in adulthood, their replenishment is thought to depend exclusively on circulating monocytes. Here, we identify a previously unrecognized CD4-lineage erythro-myeloid progenitor, termed EMPROR (Erythro-Myeloid Progenitor), that resides in the adult bone marrow and defines an alternative pathway for generating macrophages. EMPROR cells are phenotypically and transcriptionally distinct from hematopoietic stem cells, common myeloid progenitors, and monocyte precursors. They lack expression of Csf1r and Ccr2 while expressing Cd4 and c-Kit. Single-cell RNA sequencing, RNA velocity analysis, and in vitro and in vivo lineage assays demonstrate a multilineage potential encompassing macrophage, neutrophil, megakaryocytic, and erythroid fates. In vivo, EMPROR cells efficiently generate perivascular and tumor-associated macrophages independently of CCR2-mediated monocyte recruitment, and also contribute to erythroid and granulocytic lineages under inflammatory and neoplastic conditions. Transcriptomic comparisons position EMPROR cells closest to embryonic erythro-myeloid progenitors, indicating that an embryonic-like erythro-myeloid program persists within the adult bone marrow. These findings expand current models of adult myelopoiesis and highlight a previously unappreciated developmental pathway that sustains macrophage diversity beyond the classical monocyte lineage.

  单细胞
• Transcriptomic profiling of primary rat nucleus pulposus cells cultured in soft and stiff GelMA hydrogels
  GSE344937Rattus norvegicus6 个样本2026-10-30

  This study profiles gene expression in primary rat nucleus pulposus cells encapsulated in 10% GelMA hydrogels with either 30% or 60% methacryloyl substitution. Three independent biological replicates were sequenced for each matrix condition.
• RNA-bound MYBL2 engages the oncogenic transcription factors MAFG and FRA1 to promote melanoma
  GSE335104Homo sapiens9 个样本2026-10-30

  Non-mutational mechanisms, including copy number alterations and transcription factor dysregulation, are critical drivers of melanoma progression. We identify the transcription factor MYBL2 as a key oncogenic driver located on frequently amplified chromosome 20q. MYBL2 overexpression promotes transformation and correlates with poor survival, yet paradoxically, its transactivation function is dispensable for oncogenic activity. Instead, MYBL2 acquires a previously unrecognized non-canonical RNA binding function in melanoma cells enabled by the melanoma-associated RNA landscape. Through these RNA interactions, MYBL2 reshapes the chromatin landscape toward an AP-1 permissive state and promotes chromatin association of the oncogenic transcription factors MAFG and FRA1, indirectly reprogramming tumor-promoting gene networks whose expression predicts poor outcomes across multiple cancers. Importantly, disrupting the MYBL2-RNA interaction using a small decoy RNA impairs MYBL2 association with MAFG and FRA1 and suppresses melanoma cell growth. Our findings establish MYBL2 as an RNA binding-dependent, 20q gain-associated driver of melanoma and reveal that MYBL2-RNA interactions promote melanoma progression through chromatin and transcriptional network remodeling.
• RNAseq data from canine normal brain tissue
  GSE330017Canis lupus familiaris7 个样本2026-10-30

  Canine normal brain tissue samples in this dataset were utilized for comparative genomics analyses for a previously published dataset of canine gliomablastoma. These data were used to provide the first comprehensive cross-species comparison of the three canonical glioblastoma pathways – RTK/RAS/PI(3)K, p53 and Rb – across adult human, pediatric human and canine glioma, alongside in-depth characterization of the tumor microenvironment (TME).
• Detection of a sequence feature for recursive splicing
  GSE327295Homo sapiens5 个样本2026-10-30

  RNA splicing is directed by cis-acting sequence signals interacting with trans-acting factors to remove introns from newly transcribed pre-mRNA, joining exons to generate mature mRNA. Splicing happens far more often than observed exon-exon junctions in mRNA. As one contributing process, the spliceosome progressively removes large introns in small segments by ‘recursive splicing’, instead of splicing the whole intron at one time. However, the cis-acting sequences associated with recursive splicing have not been identified. Using probabilistic mixture models, we found that recursive splicing occurs more frequently in first introns, which are typically longer, and exhibit a distinct CG-rich sequence feature in the sequences flanking the upstream 5’SS, and depletion of CGs in the downstream polypyrimidine tract. Remarkably, recursive splicing is also more frequent in downstream introns of genes containing first introns with these properties. Mechanistically, these data suggest that early events in RNA synthesis and processing influence the prevalence of recursive splicing for the rest of the transcript. Finally, we developed a sequence-dependent classifier for recursive splicing, which we tested with a novel medium-throughput primer extension assay. In summary, the usage of recursive splicing sites is established at the beginning of RNA synthesis through newly-identified sequence motifs flanking both ends of the first intron.

  计算与 AI
• Aberrant stabilization of the m6A reader IGF2BP3 drives metastatic progression and 5-FU refractoriness in FBXW7-mutant colorectal cancer
  GSE326794Homo sapiens4 个样本2026-10-30

  Loss of the E3 ubiquitin ligase FBXW7 leads to aberrant stabilization of the m6A reader IGF2BP3 in colorectal cancer. To identify the RNA targets of IGF2BP3 under FBXW7-deficient conditions, we performed HITS-CLIP-seq in isogenic DLD1 FBXW7 wild-type and knockout cell lines. CLIP-seq analysis revealed that IGF2BP3-binding sites were enriched in 3' UTR regions of protein-coding mRNAs, and that IGF2BP3 preferentially bound cancer-promoting transcripts including DPYD and COL4A1.
• CRYAB-driven mitochondrial fission induces senescence to promote adaptive resistance to EGFR-TKI in LUAD brain metastasis
  GSE326531Mus musculus4 个样本2026-10-30

  Epidermal growth factor receptor tyrosine kinase inhibitors (EGFR-TKIs) exhibit limited efficacy against lung cancer brain metastases, often resulting in rapid and inevitable resistance. However, the unique mechanisms driving this brain microenvironment-specific therapeutic failure remain elusive. Here, utilizing in vivo orthotopic models and single-cell RNA sequencing, we reveal that targeted therapy induces a distinct, metabolically hyperactive senescent cell subpopulation that drives rapid EGFR-TKI tolerance in brain metastasis. We identify the molecular chaperone CRYAB as an indispensable driver specifically upregulated within this senescent persister state. Mechanistically, CRYAB physically interacts with VDAC2 at the outer mitochondrial membrane, promoting endoplasmic reticulum (ER)-mitochondria tethering and calcium influx. This CRYAB-VDAC2 axis orchestrates adaptive mitochondrial fission, hyperactivating oxidative metabolism while simultaneously shielding（preventing？） senescent cells from fatal oxidative stress. Genetic or pharmacological blockade of mitochondrial fission completely abolishes CRYAB-mediated therapeutic resistance. Therapeutically, we demonstrate that a 25-hydroxycholesterol (25HC) dietary intervention acts as a potent in vivo senolytic strategy, directly dismantling the CRYAB-dependent resistance network, eradicating senescent persister cells, and synergistically prolonging overall survival when combined with Osi. Furthermore, high baseline CRYAB expression in pre-treatment primary lung biopsies clinically predicts lower intracranial objective response rates and shorter progression-free survival in a cohort of advanced EGFR-mutant NSCLC patients. Collectively, our study uncovers a novel CRYAB-VDAC2-mitochondrial fission axis that enforces therapy-induced senescence and highlights 25HC dietary intervention as a highly translatable combinatorial strategy to overcome EGFR-TKI resistance in brain metastasis.

  单细胞
• Establishment of a multi-stage in vitro screening platform to identify candidate compounds for intestinal mucosal damage in inflammatory bowel disease
  GSE321659Homo sapiens9 个样本2026-10-30

  Mucosal healing is a key therapeutic goal in inflammatory bowel disease (IBD), which is characterized by mucosal lesions in the gastrointestinal tract. For IBD drug development, it is important to identify multiple compounds with strong effects on mucosal injury and different mechanisms of action. Here, we established an intestinal organoid-based assay to evaluate cytokine-induced inflammatory and epithelial stress responses. We also developed an intestinal microphysiological system (intestinal MPS)-based assay for quantitative evaluation of cytokine-induced changes in mucosal architecture. By integrating these assays, we constructed a multi-stage screening platform to identify candidate compounds that suppress inflammatory responses and preserve mucosal architecture. Tofacitinib, an approved IBD drug, showed positive effects in these assays, supporting the relevance of this platform. Although organoid-based screening identified pimitespib as a candidate compound, pimitespib did not improve mucosal architecture in the intestinal MPS. Consistently, pimitespib failed to restore mucosal morphology in an IBD mouse model. These findings suggest that combining intestinal organoids with an intestinal MPS may help identify candidate compounds that suppress inflammatory responses while preserving mucosal architecture.
• A Cross-scale Causal Mapping Framework Pinpoints Macrophage Orchestrators of Balanced Arterial Development
  GSE317047Homo sapiens3 个样本2026-10-30

  This dataset contains single-cell RNA sequencing profiles of induced pluripotent stem cell (iPSC)-derived blood vessel organoids (BVOs) cultured under different macrophage co-culture conditions. The aim is to investigate the regulation of vascular maturation and arterial development by the immune system. The BVOs were cultured either alone or with two polarized populations of iPSC-derived macrophages: activated (MGL low) and regenerative (MGL high). Single-cell transcriptomic analyses revealed polarization-dependent transcriptional changes in vascular endothelial and perivascular cell populations. This dataset allows for the identification of candidate genes and signaling pathways associated with arterial specification, vessel stabilization, and vascular maturation in a human organoid model.

  单细胞
• scRNAseq analysis of rat dorsal root ganglions from different peripheral injury treatment; a nerve transection, a crush 2 weeks after the cut and a resection of the neuroma 2 weeks afrer the initial cut
  GSE315353Rattus norvegicus6 个样本2026-10-30

  Peripheral nerve injury, whether caused by a cut, crush, or excessive stretch, can result in the formation of a painful neuroma at the site of damage. After a traumatic injury, regenerating nerves may develop a painful swelling at the severed end. This development is often accompanied by significant pain along the affected nerve's distribution, which can, in some cases, be more debilitating than the loss of motor function or sensation. It has been hypothesized that a proximal nerve crush may offer therapeutic benefits for painful neuromas by altering the axonal growth pattern and disrupting retrograde signaling. Despite existing treatment approaches, success in managing neuromas has been limited. Therefore, it is crucial to deepen our understanding of painful neuromas and develop more effective therapies. The molecular mechanisms underlying the formation and pain associated with symptomatic neuromas remain poorly understood. In this study, we thoroughly characterize the transcriptional changes in the dorsal root ganglion at single-cell resolution following proximal nerve crush versus nerve resection after neuronal transection.

  单细胞
• Immune cells adapt to distinct stem cell niches to govern tissue homeostasis [scRNA-seq]
  GSE314679Mus musculus2 个样本2026-10-30

  In adult tissues, epithelial stem cells exist within distinct residences, each endowing them with exclusive instructions for regenerative fitness in homeostasis and wound repair. Key components of these ‘niches’ are immune cells, which protect the host against external and internal threats. Whether and how stem cell: immune cell crosstalk contributes to normal tissue homeostasis remains less clear. Here, we discover functional adaptation of lymphocytes within two distinct skin stem cell niches and show that through this communication, each niche adjusts to meet diverse tissue demands. In the upper hair follicle, where microbial load is high, T cells express lymphotoxin-β and stimulate adjacent receptor-positive epithelial stem cells to form an immune-competent niche tailored to control microbial expansion. By contrast, in the epidermis, these T cells produce amphiregulin to maintain stem cell stoking of the skin’s barrier. Concomitantly, they express the immune checkpoint protein ‘LAG3’, which autorestricts lymphocyte numbers, and hence amphiregulin levels, thereby preventing over-proliferative responses. Finally, when epidermal T cells are absent, distinct dermal lymphocytes restore the imbalance by colonizing the niche and activating amphiregulin. Our findings unveil new modes of homeostatic control and functional specialization of immune-stem cell niches, tailoring them to suit the demands of distinct tissue microenvironments.

  单细胞
• Immune cells adapt to distinct stem cell niches to govern tissue homeostasis [bulkRNA-seq]
  GSE314678Mus musculus4 个样本2026-10-30

  In adult tissues, epithelial stem cells exist within distinct residences, each endowing them with exclusive instructions for regenerative fitness in homeostasis and wound repair. Key components of these ‘niches’ are immune cells, which protect the host against external and internal threats. Whether and how stem cell: immune cell crosstalk contributes to normal tissue homeostasis remains less clear. Here, we discover functional adaptation of lymphocytes within two distinct skin stem cell niches and show that through this communication, each niche adjusts to meet diverse tissue demands. In the upper hair follicle, where microbial load is high, T cells express lymphotoxin-β and stimulate adjacent receptor-positive epithelial stem cells to form an immune-competent niche tailored to control microbial expansion. By contrast, in the epidermis, these T cells produce amphiregulin to maintain stem cell stoking of the skin’s barrier. Concomitantly, they express the immune checkpoint protein ‘LAG3’, which autorestricts lymphocyte numbers, and hence amphiregulin levels, thereby preventing over-proliferative responses. Finally, when epidermal T cells are absent, distinct dermal lymphocytes restore the imbalance by colonizing the niche and activating amphiregulin. Our findings unveil new modes of homeostatic control and functional specialization of immune-stem cell niches, tailoring them to suit the demands of distinct tissue microenvironments.