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IL-9 is required for multi-cytokine producing tissue-resident memory CD4+ T cell-dependent allergic airway recall responses

ABSTRACT: IL-9 is required for multi-cytokine producing tissue-resident memory CD4+ T cell-dependent allergic airway recall responses

PROVIDER: PRJNA788490 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17218059.fastq.gz	Fastqsanger.gz
	SRR17218060.fastq.gz	Fastqsanger.gz
	SRR17218061.fastq.gz	Fastqsanger.gz
	SRR17218062.fastq.gz	Fastqsanger.gz
	SRR17218063.fastq.gz	Fastqsanger.gz

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IL-9 is required for multi-cytokine producing tissue-resident memory CD4+ T cell-dependent allergic airway recall responses

Project description:Asthma is a chronic inflammatory lung disease with intermittent flares predominately mediated through memory T cells. Yet, the identity of long-term memory cells that mediate allergic recall responses are not well defined. In this report, using a mouse model of chronic allergen exposure followed by an allergen-free rest period, we have characterized a sub-population of Th2 cells that secretes IL-9 as an obligate effector cytokine. IL-9-secreting cells have a resident memory T cell phenotype and blocking IL-9 during a recall challenge significantly diminishes airway inflammation and airway hyperreactivity. T cells secrete IL-9 in response to allergen recall and secretion is amplified by IL-33. Using scRNA-seq and scATAC-seq, we define the cellular identity of a distinct populations of T cells with pro-allergic cytokine patterns. Thus, in a recall model of allergic airway inflammation, IL-9 secretion from a multi-cytokine producing cell population is required for an allergen recall response.

2022-01-31 | GSE190795 | GEO

SREBP signaling regulates lung resident memory B cell metabolism to sustain allergic memory

Project description:IgE drives allergic airway disease, yet the mechanisms sustaining IgE memory remain incompletely understood. Using a murine model of allergy, we identified CCR6⁺ CD69⁺ lung-resident memory B cells (BRM) that persist after sensitization and expand rapidly upon allergen re-exposure, generating allergen-specific IgG1 and IgE. Transcriptomic analysis revealed that BRM adopt a distinct lipid metabolic program regulated by sterol regulatory element-binding protein (SREBP) signaling. Conditional deletion of this pathway revealed stage-specific roles: it is essential for GC-derived BRM formation, dispensable for maintenance, yet critical during memory recall to support BRM expansion, plasma cell differentiation, and local antibody production. Loss of SREBP signaling during memory recall impaired fatty acid metabolism, protein synthesis and effector differentiation in BRM, while also reducing plasma cell metabolic fitness, resulting in diminished IgG1 and IgE production. These findings identify a lung BRM subset as a key driver of pathogenic antibody responses and establish SREBP signaling as a stage-specific regulator of BRM, highlighting sterol pathways as potential therapeutic targets for allergic disease.

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Androgens Alleviate Allergic Airway Inflammation by Suppressing Cytokine Production of Th2 Cells

Project description:Androgens Alleviate Allergic Airway Inflammation by Suppressing Cytokine Production of Th2 Cells

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SIKs regulate HDAC7 stabilization and cytokine recall in late-stage T cell effector differentiation

Project description:Understanding the mechanisms underlying the acquisition and maintenance of effector function during T cell differentiation is important to unraveling how these processes can be dysregulated in the context of disease and manipulated for therapeutic intervention. Herein, we report the identification of a novel regulator of murine T cell differentiation through the evaluation of a previously unreported activity of the kinase inhibitor, BioE-1197. Specifically, we demonstrate liver kinase B1 (LKB1) mediated activation of salt-inducible kinases (SIKs) epigenetically regulates cytokine recall potential in effector CD8+ and Th1 cells. Evaluation of this phenotype revealed SIK mediated phosphorylation dependent stabilization of histone deacetylase 7 (HDAC7) occurred during late-stage effector differentiation. HDAC7 stabilization increased nuclear HDAC7 levels which correlated with both global and cytokine loci specific reductions in the activating transcription mark, histone 3 lysine 27 acetylation (H3K27Ac). Accordingly, HDAC7 stabilization diminished transcriptional induction of cytokine upon re-stimulation. Inhibition of this pathway during differentiation produced effector T cells epigenetically poised for enhanced cytokine recall. This work identifies a novel target for enhancing effector T cell functionality.

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Allergic airway recall responses require IL-9 from resident memory CD4<sup>+</sup> T cells.

Project description:Asthma is a chronic inflammatory lung disease with intermittent flares predominately mediated through memory T cells. Yet, the identity of long-term memory cells that mediate allergic recall responses is not well defined. In this report, using a mouse model of chronic allergen exposure followed by an allergen-free rest period, we characterized a subpopulation of CD4+ T cells that secreted IL-9 as an obligate effector cytokine. IL-9-secreting cells had a resident memory T cell phenotype, and blocking IL-9 during a recall challenge or deleting IL-9 from T cells significantly diminished airway inflammation and airway hyperreactivity. T cells secreted IL-9 in an allergen recall-specific manner, and secretion was amplified by IL-33. Using scRNA-seq and scATAC-seq, we defined the cellular identity of a distinct population of T cells with a proallergic cytokine pattern. Thus, in a recall model of allergic airway inflammation, IL-9 secretion from a multicytokine-producing CD4+ T cell population was required for an allergen recall response.

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Project description:Group 2 innate lymphoid cells (ILC2s) have tissue-resident competence and contribute to the pathogenesis of allergic diseases. Therefore, there should be mechanisms to maintain the capacity of ILC2s to produce TH2 cytokines under chronic inflammatory conditions. Here, we report that Runx proteins are essential to prevent exaggerated activation of ILC2, in part by antagonizing GATA-3 function at steady state. However, during allergic inflammation, the absence of Runx in ILC2s impaired their ability to proliferate and produce effector TH2 cytokines and chemokines, but instead induced expression of T cell exhaustion markers including IL-10 and TIGIT. These exhausted ILC2s were unabale to induce type 2 immune responses against repeated allergen inhalation. Thus, Runx proteins protect ILC2s from exhaustion during continuous allergic inflammation.

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Project description:Obesity is associated with severe, difficult to control asthma, and increased airway oxidative stress. Mitochondrial reactive oxygen species (mROS) are an important source of oxidative stress leading us to hypothesize that targeting mROS in obese allergic asthma might be an effective treatment strategy. Using a mouse model of house dust mite (HDM) induced allergic airway disease in mice fed a low- (LFD) or high-fat diet (HFD), and the mitochondrial antioxidant MitoQuinone (MitoQ); we investigated the effects of obesity and mROS on airway inflammation, remodelling and airway hyperreactivity (AHR). HDM induces airway inflammation, remodelling and hyperreactivity in both lean and obese mice. Obese allergic mice showed increased lung tissue eotaxin levels, airway tissue eosinophilia and AHR when compared to lean allergic mice. MitoQ reduced markers of airway inflammation, remodelling and hyperreactivity in both lean and obese allergic mice, and tissue eosinophilia in obeseHDM mice. mROS regulates cell signalling by protein oxidation of multiple downstream targets: MitoQ reduced HDM-induced cysteine-sulfenylation of several proteins including those involved in the unfolded protein response (UPR). In summary, mROS mediates the development of allergic airway disease and hence MitoQ might be effective for the treatment for asthma, and specific features of obese asthma.

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Distinct functions of tissue-resident and circulating memory Th2 cells in allergic airway disease

Project description:Distinct functions of tissue-resident and circulating memory Th2 cells in allergic airway disease

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CD4+ resident memory T cells dominate immunosurveillance and orchestrate local recall responses

Project description:CD4+ resident memory T cells dominate immunosurveillance and orchestrate local recall responses

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