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M2-like dermis resident macrophages regulate type 1 2 circuitries with ILC2s and eosinophils to exacerbate cutaneous leishmaniasis

ABSTRACT: Tissue-resident macrophages (TRMs) are critical for tissue homeostasis/repair. We previously showed that dermal TRMs produce CCL24 which mediates their interaction with IL-4 producing eosinophils, required to maintain their M2-like properties in the TH1 environment of the Leishmania major infected skin. Here, we unveil another layer of TRM self-maintenance involving production of TSLP, an alarmin typically characterized as epithelial cell-derived. Both TSLP signaling and IL-5+ innate lymphoid cell 2 (ILC2s) were shown to maintain dermal TRM numbers and promote infection. Single cell RNA sequencing identified the dermal TRMs as the sole source of TSLP and CCL24. Generation of Ccl24-cre mice permitted specific labeling of dermal TRMs, as well as interstitial TRMs from other organs. Genetic ablation of TSLP from dermal TRMs reduced the number of dermal TRMs and ameliorated infection. Here, we show that by orchestrating localized type 2 circuitries with ILC2s and eosinophils, dermal TRMs are self-maintained as a replicative niche for L. major.

ORGANISM(S): Mus musculus

PROVIDER: GSE243853 | GEO | 2023/10/30

REPOSITORIES: GEO

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Fibrosis induced by resident macrophages has divergent roles in pancreas inflammatory injury and PDAC

Project description:Tissue-resident macrophages (TRMs) are long-lived cells that maintain locally and can be phenotypically distinct from monocyte-derived macrophages. Whether TRMs and monocyte-derived macrophages have district roles under differing pathologies is not understood. Here, we showed that a substantial portion of the macrophages that accumulated during pancreatitis and pancreatic cancer in mice had expanded from TRMs. Pancreas TRMs had an extracellular matrix remodeling phenotype that was important for maintaining tissue homeostasis during inflammation. Loss of TRMs led to exacerbation of severe pancreatitis and death, due to impaired acinar cell survival and recovery. During pancreatitis, TRMs elicited protective effects by triggering the accumulation and activation of fibroblasts, which was necessary for initiating fibrosis as a wound healing response. The same TRM-driven fibrosis, however, drove pancreas cancer pathogenesis and progression. Together, these findings indicate that TRMs play divergent roles in the pathogenesis of pancreatitis and cancer through regulation of stromagenesis.

2023-06-29 | GSE203005 | GEO

Fibrosis induced by resident macrophages has divergent roles in pancreas inflammatory injury and PDAC

2023-06-29 | GSE196778 | GEO

Cognate antigen-independent differentiation of resident memory t cells in chronic kidney disease

Project description:Although resident memory T cells (TRMs), which are memory T cells that are retained locally within tissues, have recently been described as antigen-specific frontline defenders against pathogens in barrier and non-barrier epithelial tissues, they have also been noted for perpetuating chronic inflammation. Furthermore, the conditions responsible for TRM differentiation are still poorly understood, and their contributions, if any, to sterile models of chronic kidney disease (CKD) remain a mystery. In this study we identify a substantial population of TRMs in the kidneys of mice with aristolochic acid (AA)-induced CKD. Flow cytometry of injured kidneys showed T cells bearing TRM surface markers and single cell RNA sequencing revealed these cells as expressing well-known TRM transcription factors and receptors responsible for TRM differentiation and maintenance. While kidney TRMs expressed Cd44, a marker of antigen experience and T cell activation, their derivation was surprisingly independent of cognate antigen-T cell receptor interactions, as the kidneys of transgenic OT-1 mice still harbored considerable proportions of TRMs after injury. Our results suggest a non-antigen-specific or antigen-independent mechanism capable of generating TRMs in the kidney and highlight the need to better understand TRMs and their involvement in CKD.

2024-03-01 | GSE246803 | GEO

The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [scRNA-Seq]

Project description:Tissue-resident macrophages (TRMs) play central roles in local tissue development and immunity. However, how to control TRM ontogeny and maintenance remains unclear. We performed transcriptional and histone modification analyses of alveolar macrophages in mice with myeloid-specific (Csf1rCre) deletion of HDAC3 using bulk RNA-seq, single-cell RNA-seq and ChIP-seq. We report that HDAC3 deficiency results in metabolic disorders and increased cell death of the fetal lung TRMs, which is partially regulated through directly targeting PPAR-γ. Although the loss of AMs in the absence of HDAC3 is not AM subset specific, the transcriptome changes in HDAC3 deficient AM subsets are different. We propose that HDAC3 serves a key epigenetic regulator that controls embryonic TRM ontogeny and maintenance.

2020-09-22 | GSE122529 | GEO

The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [ChIP-Seq]

2020-06-23 | GSE122532 | GEO

The epigenetic regulator Histone Deacetylase 3 regulates the ontogeny and maintenance of tissue-resident macrophage [RNA-Seq]

2020-06-23 | GSE122393 | GEO

Eosinophils promote effector functions of lung ILC2s in allergic airway inflammation in mice

Project description:We investigated reciprocal interactions between cocultures of isolated populations of eosinophils and ILC2s and found these cells promote changes in gene expression as compared to being cultured alone.

2023-04-07 | GSE220453 | GEO

Adventitial stromal cells define group 2 innate lymphoid cell tissue niches

Project description:We identify a subset of IL-33 expressing adventitial stromal cells as local regulators of ILC2s Type 2 lymphocytes promote both physiologic tissue remodeling and allergic pathology, yet their physical tissue niches are poorly described. In this study, we used quantitative imaging together with scRNAseq to define tissue niches of group 2 innate lymphoid cells (ILC2s), critical instigators of type 2 immunity. We identified a dominant adventitial cuff niche around lung bronchi and larger vessels in multiple tissues, where ILC2s localized with subsets of dendritic and regulatory T cells. However, ILC2s were most intimately associated with adventitial stromal cells (ASC), a mesenchymal fibroblast-like subset that expressed Interleukin-33 (IL-33) and thymic stromal lymphopoietin (TSLP) and supported ILC2s and tissue-resident Th2 cells.

2019-03-31 | GSE125492 | GEO

Tissue signals imprint ILC2 identity with anticipatory function [single cell RNA-Seq]

Project description:Group 2 innate lymphoid cells (ILC2s) are distributed systemically and produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Transcriptional profiling of ILC2s from different tissues, however, grouped ILC2s according to their tissue of origin, even in the setting of combined IL-25, IL-33R and TSLPR-deficiency. Single-cell profiling confirmed a tissue-organizing transcriptome and identified ILC2 subsets expressing distinct activating receptors, including the major subset of skin ILC2s, which were activated preferentially by IL-18. Tissue ILC2 subsets were normal in germ- free mice, suggesting that endogenous, tissue-derived, signals drive the maturation of ILC2 subsets by controlling expression of distinct patterns of activating receptors, thus anticipating tissue-specific patterns to perturbations occurring later in life.

2018-09-10 | GSE117567 | GEO

Tissue signals imprint ILC2 identity with anticipatory function [RNA-Seq]

2018-09-10 | GSE117470 | GEO

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