Publications by authors named "Darryl J Mar"

Article Synopsis
  • IL-31, a cytokine linked to itchy skin diseases, has complex effects on inflammation and neuro pathways, which are not fully understood.
  • In a mouse model, disrupting IL-31 reduced scratching associated with allergic dermatitis, suggesting it usually promotes itching, while the absence of its receptor increased certain immune responses like T cell activation and IgE production.
  • The study reveals that IL-31 acts more as an immunoregulatory factor, potentially limiting inflammation by triggering specific neuro pathways, which could explain dermatitis flare-ups in patients receiving treatments against IL-31 receptor.
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Coordinate control of T cell proliferation, survival, and differentiation are essential for host protection from pathogens and cancer. Long-lived memory cells, whose precursors are formed during the initial immunological insult, provide protection from future encounters, and their generation is the goal of many vaccination strategies. microRNAs (miRNAs) are key nodes in regulatory networks that shape effective T cell responses through the fine-tuning of thousands of genes.

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Extracellular RNAs (exRNAs) can be released by numerous cell types in vitro, are often protected within vesicles, and can modify recipient cell function. To determine how the composition and cellular sources of exRNAs and the extracellular vesicles (EVs) that carry them change in vivo during tissue inflammation, we analyzed bronchoalveolar lavage fluid (BALF) from mice before and after lung allergen challenge. In the lung, extracellular microRNAs (ex-miRNAs) had a composition that was highly correlated with airway-lining epithelium.

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Chronic glucocorticoid exposure is associated with the development of insulin resistance. We showed that glucocorticoid-induced insulin resistance was attenuated upon ablation of , a glucocorticoid target gene encoding the secreted protein angiopoietin-like 4, which mediates glucocorticoid-induced lipolysis in white adipose tissue. Through metabolomic profiling, we revealed that glucocorticoid treatment increased hepatic ceramide concentrations by inducing enzymes in the ceramide synthetic pathway in an Angptl4-dependent manner.

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