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Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [ex_vivo_ILC2]

ABSTRACT: The goal of this study was to determine whether thymic innate lymphoid cells type-2 (ILC2) activation during acute thymic involution is mediated by the alarmins IL-25 and IL-33. For this purpose we sorted thymic ILC2 from WT mice, treated them ex vivo with recombinant IL-25/IL-33 or both for 24 hours, and performed bulk RNA Seq.

ORGANISM(S): Mus musculus

PROVIDER: GSE244222 | GEO | 2024/01/11

REPOSITORIES: GEO

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Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [ILC2_after_Dex]

Project description:The goal of this study was to understand the role of thymic innate lymphoid cells (ILC2) in thymic regeneration following dexamethasone-induced acute involution, and determine whether this is activated by the alarmins IL-25 and IL-33. For this purpose we treated WT, Il25 KO or Il33 mice with dexamethasone, sorted ILC2 cells from their thymi 3 days after treatment when the thymus begins its recovery, or at an earlier time point (18 hours) for comparison, and performed bulk RNA-Seq.

2024-01-11 | GSE244216 | GEO

Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [ILC2_after_irr]

Project description:The goal of this study was to understand the role of thymic innate lymphoid cells (ILC2) in thymic regeneration following irradiation-induced acute involution, and determine whether this is activated by the alarmin IL-25. For this purpose we treated WT or Il25 KO mice with sublethal irradiation and/or recombinant IL-25, sorted ILC2 cells from their thymi 3 days after treatment when the thymus begins its recovery, and performed bulk RNA Seq.

2024-01-11 | GSE244202 | GEO

Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [ex_vivo_tuft]

Project description:The goal of this study was to determine whether thymic tuft cells activation during acute thymic involution is mediated by IL-13, which is produced by ILC2 upon involution and the receptor for which is expressed by tuft cells. For this purpose we sorted thymic tuft cells from WT mice, treated them ex vivo with recombinant IL-13 for 24 hours, and performed bulk RNA-Seq.

2024-01-11 | GSE244223 | GEO

Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [IL25KO_ILC2_untreated]

Project description:The goal of this study was to determine whether the alarmin IL-25 has an effect on thymic innate lymphoid cells type-2 (ILC2) at steady state. For this purpose we sorted thymic ILC2 from WT or Il25 KO mice and performed bulk RNA-Seq.

2024-01-11 | GSE244224 | GEO

Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [Tuft_after_Dex]

Project description:The goal of this study was to understand the role of thymic tuft cells in thymic regeneration following dexamethasone-induced acute involution, and determine whether this is affected by IL-13, which is produced by ILC2 upon involution and the receptor for which is expressed by tuft cells. For this purpose we treated WT and Il13ra1 KO mice with dexamethasone, sorted tuft cells from their thymi 3 days after treatment when the thymus begins its recovery, at an earlier time point (18 hours) for comparison, or at a later time point (6d) when IL-13 has been released, and performed bulk RNA Seq.

2024-01-11 | GSE244220 | GEO

Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [TEC_after_rAREG_inj]

Project description:The goal of this study was to determine how thymic epithelial cells (TEC) differentiation and gene expression is affected by amphiregulin (AREG), which is produced by ILC2 upon thymic involution and the receptor for which is expressed by early TEC subsets. For this purpose we treated WT mice with recombinant AREG, sorted TEC from their thymi 10 days after treatment when the thymus is recovering and AREG has been released, and performed bulk RNA-Seq.

2024-01-11 | GSE244225 | GEO

mRNA-seq of thymic epithelial cells from PBS or IL-33 treated thymus

Project description:Severe infection commonly results in T cell aging, which leads to impaired pathogen clearance or increased secondary infection in both humans and animals. However, the exact mechanisms remain poorly understood. Here, we demonstrated that severe infection-induced IL-33 production resulted in acute thymic involution-mediated naive T cell aging and impaired host control of infection in mouse disease models of schistosomiasis or sepsis. Furthermore, we illustrated that IL-33 triggered excessive generation of medullary thymic epithelial cell (mTEC) IV (thymic tuft cells) in a Pou2f3-dependent manner, as a consequence, disturbed mTEC/cortical TEC (cTEC) compartment and caused acute thymic involution during severe infection. More importantly, IL-33 deficiency or IL-33 receptor ST2 deficient thymus transplantation rescued T-cell immunity to better control infection in mice. Our findings not only uncover a novel link between severe infection-induced IL-33 and thymic involution-mediated naive T cell aging, but also suggest that targeting IL-33 or ST2 is a promising strategy to rejuvenate T cell immunity to better control severe infection.

2022-10-23 | GSE189201 | GEO

Tuft cells and fibroblasts promote thymus regeneration through activation of a type-2 immune response [Tuft_after_irr]

Project description:The goal of this study was to understand the role of thymic tuft cells in thymic regeneration following irradiation-induced acute involution. For this purpose we treated WT mice with sublethal irradiation, sorted tuft cells from their thymi 3 days after treatment when the thymus begins its recovery, and performed bulk RNA Seq.

2024-01-11 | GSE244219 | GEO

Human ILC2 cells stimulated with IL-25, IL-33, or TSLP

Project description:ILC2 cells are a newly described cell type whose biology and contribution to disease are poorly understood. ILC2 cells are activated by allergens, viral infection, and/or epithelial damage via IL-33 and IL-25. ILC2 cells require IL-2, IL-7, IL-25 and IL-33 for their survival and expansion. In mice, ILC2s produce multiple mediators primarily associated with type 2 inflammation (IL-13, IL-5, IL-4, IL-6, IL-9, IL-10, GM-CSF, amphiregulin). ILC2 cells may contribute to the pathology of asthma through multiple mediators that include IL-13-independent pathways. Our goal is to compare transcriptional profiles of IL-33- or IL-25-activated ILC2 cells from blood to characterize these cells and to identify marker(s) that can be utilized to detect them in human tissue. ILC2 cells (Lineage negative, CRTH2+, CD161+, CD127+) were purified from human blood of 5 different donors by flow cytometry. The ILC2 yield ranged from 20,000 to 165,000 cells per donor (0.001-0.008% WBC). Purified ILC2s were expanded in vitro in the presence of IL-2, IL-7, IL-33 and IL-25 (each at 50 ng/ml) for 7-10 days. Expanded cells maintained the ILC2 phenotype (Lineage negative, CRTH2+, CD161+, CD127+). The cells were rested for 2 days in the presence of 1 ng/ml IL-2 and IL-7 and then treated in the presence of 1 ng/ml IL-2 and IL-7 with either media control, IL-25 (50 ng/ml), IL-33 (50 ng/ml), and/or TSLP (50 ng/ml) in combination, for 6 or 24 hours. Whole RNA was isolated via the RNeasy kit (Qiagen). Stratagene Universal Human Reference RNA was used as the reference.

2013-12-31 | E-GEOD-45458 | biostudies-arrayexpress

Transcriptome of Chat positive and negative ILC2s

Project description:Group 2 innate lymphoid cells (ILC2s) reside in multiple tissues including lymphoid organs and barrier surfaces, and secrete type 2 cytokines including interleukin (IL)-5, IL-9 and IL-13. These cells participate in multiple physiological processes including allergic inflammation, tissue repair, metabolic homeostasis and host defense against helminth infections. Recent studies indicate that neuropeptides can play an important role in regulating ILC2 responses, however, the mechanisms that underlie these processes in vivo remain incompletely defined. Here, we identify that activated ILC2s upregulate choline acetyltransferase (ChAT)—the enzyme responsible for the biosynthesis of acetylcholine (ACh)—following infection with the helminth parasite Nippostrongylus brasiliensis or treatment with alarmins or cytokines including IL-25, IL-33 and thymic stromal lymphopoietin (TSLP). ILC2s also express acetylcholine receptors (AChRs), and ACh administration promotes ILC2 cytokine production and elicits expulsion of helminth infection. In accordance with this, ChAT deficiency in ILC2s leads to defective ILC2 responses and impaired immunity against helminth infection. Together, these results reveal a previously unrecognized role of the ChAT-ACh pathway in promoting type 2 innate immunity to helminth infection.

2021-03-05 | GSE164705 | GEO

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