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Bucar, E. B.

Publications and source records attributed to Bucar, E. B..

2 recordsLinked to original sources

Dysregulation of γδ intraepithelial lymphocytes precedes Crohn's disease-like ileitis

Intraepithelial lymphocytes expressing the {gamma}{delta} T cell receptor ({gamma}{delta} IELs) provide immunosurveillance of the intestinal barrier. Interestingly, {gamma}{delta} IEL number is reduced in patients with active Crohns disease (CD). Here, we report an underappreciated role for {gamma}{delta} IELs in maintaining mucosal tolerance during the onset and progression of CD-like ileitis using the TNF{Delta}ARE/+ mouse model. Decreased epithelial HNF4G/BTNL expression is followed by a loss of ileal {gamma}{delta} IELs and impaired barrier surveillance prior to the histological onset of disease. A reduction of immunoregulatory CD39+ {gamma}{delta} IELs coincides with the influx of immature, peripheral CD39- {gamma}{delta} T cells into the epithelium leading to an expansion of induced IELs, while an earlier depletion of {gamma}{delta} IELs correlates with accelerated onset of ileal inflammation. Our findings identify multiple layers of {gamma}{delta} IEL dysregulation prior to ileitis development indicating that the loss of tissue-resident immunoregulatory {gamma}{delta} IELs may contribute to the initiation of ileal CD.

immunology↗

Sprouty2 limits intestinal tuft and goblet cell numbers through GSK3β-mediated restriction of epithelial IL-33.

Dynamic regulation of intestinal cell differentiation is crucial for both homeostasis and the response to injury or inflammation. Sprouty2, an intracellular signaling regulator, controls pathways including PI3K and MAPKs that are implicated in differentiation and are dysregulated in inflammatory bowel disease. Here, we asked whether Sprouty2 controls secretory cell differentiation and the response to colitis. We report that colonic epithelial Sprouty2 deletion led to expanded goblet and tuft cell populations. Sprouty2 loss induced PI3K/Akt signaling, leading to GSK3{beta} inhibition and epithelial interleukin (IL)-33 expression. In vivo, this resulted in increased stromal IL-13+ cells. IL-13 in turn induced tuft and goblet cell expansion in vitro and in vivo. Sprouty2 was downregulated by inflammation; this appeared to be a protective response, as VillinCre;Sprouty2F/F mice were resistant to DSS colitis. In contrast, Sprouty2 was elevated in colons of inflammatory bowel disease patients, suggesting that this protective epithelial-stromal signaling mechanism is lost in disease.

physiology↗