Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1057434 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Neuro-immune circuits regulate innate and adaptive immunity at barrier surfaces, however the differential impact of these circuits on proinflammatory versus tissue-protective responses remains poorly defined. We identify that enteric neurons produce CGRP-related adrenomedullin 2 (ADM2), and identify a previously unrecognized role for the ADM2-ADM2 receptor pathway in promoting intestinal tissue-protective functions of group 2 innate lymphoid cells (ILC2s). Genomic or ILC2-intrinsic deletion of ADM2 receptor subunits resulted in a significant reduction in tissue-protective ILC2 responses, defective amphiregulin (AREG) production and increased susceptibility to intestinal damage and inflammation. Conversely, therapeutic delivery of recombinant ADM2 elicited tissue-protective AREG production in ILC2s and limited intestinal inflammation. Expression of genes encoding human ADM2 receptor (CALCRL and RAMP3) was altered in IBD patients and associated with reduced expression of AREG in ILC2s. Collectively, these findings identify that the ADM2-ADM2 receptor pathway can promote tissue-protective functions of ILC2s in the context of intestinal damage and inflammation.
2025-06-25 | GSE271362 | GEO
Project description:Innate lymphoid cells (ILC) in the small intestine govern immune homeostasis and protect the host against gut pathogens. While distinct cell-intrinsic signals have been identified that determine ILC development and differentiation, it has remained unclear which cell population regulates ILC sustenance. Using unbiased single cell RNA transcriptomic analysis of intestinal fibroblasts, we have identified a specialized Ccl19-expressing fibroblastic reticular cell (FRC) population that underpins solitary intestinal lymphoid tissue (SILT) structures including cryptopatches and isolated lymphoid follicles. Conditional ablation of lymphotoxin-β receptor (LTβR) signalling in SILT FRC impeded the maturation of isolated lymphoid follicles and blocked ILC maintenance through the downregulation of IL-7, consequently resulting in the elevated susceptibility to bacterial infection. Moreover, specific Ltbr ablation in FRC during adulthood revealed that constant LTβR-dependent FRC-ILC interaction is required to maintain SILT structures and ILC populations. Taken together, our study unveils a critical intestinal FRC niche that secures protective gut immunity.
2022-02-12 | E-MTAB-10645 | biostudies-arrayexpress
Project description:Innate lymphoid cells (ILC) in the small intestine govern immune homeostasis and protect the host against gut pathogens. While distinct cell-intrinsic signals have been identified that determine ILC development and differentiation, it has remained unclear which cell population regulates ILC sustenance. Using unbiased single cell RNA transcriptomic analysis of intestinal fibroblasts, we have identified a specialized Ccl19-expressing fibroblastic reticular cell (FRC) population that underpins solitary intestinal lymphoid tissue (SILT) structures including cryptopatches and isolated lymphoid follicles. Conditional ablation of lymphotoxin-β receptor (LTβR) signalling in SILT FRC impeded the maturation of isolated lymphoid follicles and blocked ILC maintenance through the downregulation of IL-7, consequently resulting in the elevated susceptibility to bacterial infection. Moreover, specific Ltbr ablation in FRC during adulthood revealed that constant LTβR-dependent FRC-ILC interaction is required to maintain SILT structures and ILC populations. Taken together, our study unveils a critical intestinal FRC niche that secures protective gut immunity.
2022-02-12 | E-MTAB-10638 | biostudies-arrayexpress
Project description:Innate lymphoid cells (ILC) are tissue-resident effector cells with important roles in tissue homeostasis, protective immunity and inflammatory disease. Here we investigated the role of the transcription factor Bcl6 in small intestinal innate lymphoid cells. Specifically, we performed single-cell RNA-seq on total small intestine lamina propria ILCs from tamoxifen-treated Id2-CreERT2 ROSA26-tdRFP Bcl6-fl/fl mice and Id2-CreERT2 ROSA26-tdRFP controls.
2023-10-31 | E-MTAB-12864 | biostudies-arrayexpress
Project description:Interleukin-(IL) 22 production by intestinal group 3 innate lymphoid cells (ILC3) is critical to maintain gut homeostasis. However, IL-22 needs to be tightly controlled; reduced IL-22 expression is associated with intestinal epithelial barrier defect while its overexpression promotes tumor development. Here, using a single cell RNAseq approach, we identified a core set of genes associated with increased IL-22 production by ILC3.
2025-02-28 | GSE255270 | GEO
Project description:Intestinal fibroblastic reticular cell niches control innate lymphoid cell homeostasis and function - Innate lymphoid cells
| PRJEB46051 | ENA
Project description:Emerging studies reveal that neuropeptides play critical role in regulating anti-helminth immune responses, hinting at the potential of intrinsic enteric neurons (iENs) in orchestrating intestinal immunity. However, whether and how the iENs get activated during infection, and whether they engage in a bi-directional communication with the immune cells, remain poorly defined. Here we show that iENs became activated in response to helminth infection. Single-nucleus RNA sequencing of the iENs revealed significant alterations in gene expression in IL-13R+ intrinsic primary afferent neurons (IPANs), including the upregulation of the neuropeptide -CGRP. Using genetic mouse models, we demonstrated that both group 2 innate lymphoid cells (ILC2s) and neuronal IL-13R signaling are indispensable for optimal iEN activation, which subsequently inhibit ILC2 responses and anti-helminth immunity. Together, these results reveal a previously unrecognized bi-directional neuro-immune crosstalk in the intestine.
2025-01-31 | GSE260708 | GEO
Project description:Group 3 Innate Lymphoid Cells (ILC3s) is important for maintaining intestinal homeostasis and host defense. Emerging studies have shown that metabolic regulation plays a crucial role in regulating ILC3 activation and function. However, the role of Liver Kinase B1 (LKB1), key metabolic regulator, in regulating ILC3 function and intestinal immunity remains poorly understood. In this study, we show that LKB1 is essential for ILC3 postnatal development, effector function, and intestinal immunity. Ablation of LKB1 in ILC3s results in reduced cell number due to increased apoptosis and reduced proliferation, which occurs at 2 -3 weeks after birth. In addition, LKB1 deletion leads to diminished IL-22 production and less protection against C.rodentium infection. Mechanistically, LKB1 deficiency led to impaired mitochondrial metabolism, as indicated by reduced glycolysis and oxidative phosphorylation and less mitochondrial mass. Together, our data demonstrate that LKB1 promotes ILC3 postnatal development and effector function to maintain intestinal immune homeostasis.
2025-06-25 | GSE284792 | GEO
Project description:Signals from sympathetic neurons and immune cells regulate adipocytes contributing to fat tissue biology. Interactions between the nervous and immune systems have recently emerged as major regulators of host defence and inflammation1-4. Nevertheless, whether neuronal and immune cells cooperate in brain-body axes to orchestrate metabolism and obesity remains elusive. Here we report a novel neuro-mesenchyme unit that controls group 2 innate lymphoid cells (ILC2), adipose tissue physiology, metabolism and obesity via a brain-adipose circuit. We found that sympathetic nerve terminals act on neighbouring adipose mesenchymal cells via the beta-2 adrenergic receptor to control the expression of the glial-derived neurotrophic factor (GDNF) and the activity of ILC2 in gonadal fat. Accordingly, ILC2-autonomous manipulation of the GDNF receptor machinery led to altered ILC2 function, energy expenditure, insulin resistance and propensity to obesity. Retrograde tracing, chemical, surgical and chemogenetic manipulations identified a sympathetic aorticorenal circuit that modulates gonadal fat ILC2 and connects to high-order brain areas, including the paraventricular nucleus of the hypothalamus (PVH). Our work decodes a neuro-mesenchymal unit that translates long-range neuronal circuitry cues into adipose-resident ILC2 function, shaping the host metabolism and obesity.
2021-07-07 | GSE179551 | GEO
Project description:Signals from sympathetic neurons and immune cells regulate adipocytes contributing to fat tissue biology. Interactions between the nervous and immune systems have recently emerged as major regulators of host defence and inflammation1-4. Nevertheless, whether neuronal and immune cells cooperate in brain-body axes to orchestrate metabolism and obesity remains elusive. Here we report a novel neuro-mesenchyme unit that controls group 2 innate lymphoid cells (ILC2), adipose tissue physiology, metabolism and obesity via a brain-adipose circuit. We found that sympathetic nerve terminals act on neighbouring adipose mesenchymal cells via the beta-2 adrenergic receptor to control the expression of the glial-derived neurotrophic factor (GDNF) and the activity of ILC2 in gonadal fat. Accordingly, ILC2-autonomous manipulation of the GDNF receptor machinery led to altered ILC2 function, energy expenditure, insulin resistance and propensity to obesity. Retrograde tracing, chemical, surgical and chemogenetic manipulations identified a sympathetic aorticorenal circuit that modulates gonadal fat ILC2 and connects to high-order brain areas, including the paraventricular nucleus of the hypothalamus (PVH). Our work decodes a neuro-mesenchymal unit that translates long-range neuronal circuitry cues into adipose-resident ILC2 function, shaping the host metabolism and obesity.
2021-07-07 | GSE179546 | GEO