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Topical glucocorticosteroids inhibit allergic skin inflammation but are ineffective in impeding the formation and expansion of resident memory T cells

ABSTRACT: Topical glucocorticosteroids inhibit allergic skin inflammation but are ineffective in impeding the formation and expansion of resident memory T cells

PROVIDER: PRJNA895049 | ENA |

REPOSITORIES: ENA

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Topical glucocorticosteroids inhibit allergic skin inflammation but are ineffective in impeding the formation and expansion of resident memory T cells

Project description:Tissue-resident memory T (TRM) cells are detrimental in numerous chronic inflammatory diseases, including allergic contact dermatitis (ACD), in which they contribute to the chronicity and severity of the disease. We assessed the impact of a standard glucocorticosteroid treatment, triamcinolone acetonide (TA), on the formation, maintenance and reactivation of epidermal TRM cells in ACD.

2023-08-31 | GSE216725 | GEO

Normal and ineffective erythropoiesis scRNA seq

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Treatment of C3H/HeJ grafted mice with baricitinib [topical]

Project description:The C3H/HeJ grafted model of alopecia areata was used to determine the efficacy of systemic baricitinib at preventing alopecia or treating established disease. The efficacy of topical baricitinib at treating established alopecia in the C3H/HeJ grafted model was also assessed. Microarrays were performed on skin RNA at week 0 and week 12 after starting treatment in all models. Baricitinib was administered in topical form after disease establishement. Skin samples were taken at the start of treatment and after 12 weeks.

2015-05-01 | E-GEOD-61554 | biostudies-arrayexpress

A regulatory CD9+ B cell subset controls HDM-induced allergic airway inflammation

Project description:Background: A specific subset of regulatory IL-10 producing B cells has been extensively studied in autoimmune and inflammatory pathologies. These cells are able to constrain exacerbated inflammation by inhibiting T cell mediated responses and maturation of antigen presenting cells. In allergic diseases, observations that increase of regulatory B cells is necessary for allergen tolerance suggest that development of allergic asthma would be associated with a defect in the regulatory B cells compartment. Objective: We sought to (i) characterize regulatory IL-10+ regulatory B cell subset in Balb/c mice by microarray and flow cytometry and (ii) investigate their regulatory capacity in vivo in a house dust mite model of allergic asthma. Results: We identified an IL-10 producing B cells subset able to control T cell proliferation in vitro in both control and asthmatic mice. This subset is decreased in allergic mice. IL-10+ Breg cells express high levels of CD9 and upregulate CD70 and CD73 after activation. Expression of CD9 allows identifying more than 50% of Bregs. Interestingly CD9+ B cells inhibit TH2-TH17 allergic airway inflammation in vivo after adoptive transfer in an IL-10 dependent manner. Conclusions: Herein, we demonstrate that induction of allergic asthma dampens the generation of Bregs contributing to exacerbated airway inflammation. We identified a distinct CD9+ Breg-cell population decreased in lung of HDM mice and able to control asthma and allergic airway inflammation by producing IL-10 after adoptive transfer. This study points B cells as an interesting therapeutic target in allergic asthma. IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) in control mice + IL-10+ B cells (n=3) and 3 IL-10- B cells (n=3) from asthmatic allergic (HDM) mice

2015-03-01 | E-GEOD-57772 | biostudies-arrayexpress

Targeting mitochondrial reactive oxygen species alleviates allergic airway disease in a mouse model of obese allergic asthma

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.

2023-06-02 | PXD029715 | Pride

Treatment of established mouse AA with topical JAK inhibitors

Project description:Our goal was to identify gene expression patterns that correlated with treatment of established autoimmune alopecia in C3H/HeJ mice following alopecic graft transplantation skin from 3 mice were taken at 6, 12 and, in some cases, 24 weeks of topical drug administration following grafting; mice were treated with ruxolitinib (jak1i), tofacitinib (jak3i), or control pbs 3 biological replicates were taken at each time point for each treatment modality

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The pathology of ineffective erythropoiesis in Rpl11 haploinsufficienct mice

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A regulatory CD9+ B cell subset controls HDM-induced allergic airway inflammation

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Itaconate suppresses atherosclerosis by impeding inflammation through Nrf2 signaling

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