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epithelial cells

Androgen Receptor Signaling Promotes Treg Suppressive Function during Allergic Airway Inflammation

[Journal of Clinical Investigation] Using androgen receptor (AR) deficient and Foxp3 fate-mapping mice, researchers determined that AR signaling increased Treg suppression during Alternaria extract challenge by stabilizing Foxp3+ Tregs and limiting the number of ST2+ ex-Tregs and IL-13+ Th2 and ex-Tregs.

Long Noncoding RNA HOTAIRM1 Promotes Immunosuppression in Sepsis by Inducing T Cell Exhaustion

[Journal of Immunology] Using a mouse model of sepsis, scientists found that the long noncoding RNA HOXA transcript antisense RNA myeloid-specific 1 (HOTAIRM1) was highly expressed in mice during the late phase of sepsis.

Kinesin-Directed Secretion of Basement Membrane Proteins to a Subdomain of the Basolateral Surface in Drosophila Epithelial Cells

[Current Biology] Using the Drosophila follicular epithelium, researchers showed that kinesin-3 and kinesin-1 motors worked together to define this secretion site.

Cryptococcus neoformans in Association with Dermatophagoides pteronyssinus Has Pro- (IL-6/STAT3 Overproduction) and Anti-inflammatory (CCL2/ERK1/2 Downregulation) Effects on Human Bronchial Epithelial Cells

[Inflammation] The authors evaluated the effects of the association between Cryptococcus neoformans and Dermatophagoides pteronyssinus in the modulation of airway inflammatory responses in an in vitro experimental model using human bronchial epithelial cells.

Overexpression of miR-375 Reverses the Effects of Dexamethasone on the Viability, Migration, Invasion and Apoptosis of Human Airway Epithelial Cells by Targeting DUSP6

[International Journal of Molecular Medicine] The altered expression of microRNAs has been found in asthma. However, the detailed mechanisms responsible for the effects of miR‑375 on Dex‑induced airway epithelial cell dysfunction remain elusive. Researchers elucidated these mechanisms.

CDC42 Controlled Apical-Basal Polarity Regulates Intestinal Stem Cell to Transit Amplifying Cell Fate Transition via YAP-EGF-mTOR Signaling

[Cell Reports] The authors found that CDC42 loss initiated in the intestinal stem cell caused a drastic hyperproliferation of transit amplifying cells and disrupted epithelial polarity.

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