id	author	title	date	pages	extension	mime	words	sentences	flesch	summary	cache	txt
cord-304066-rirbdhz3	Reddehase, Matthias J.	Adverse immunological imprinting by cytomegalovirus sensitizing for allergic airway disease	2019-05-10		.txt	text/plain	1894	99	42	Specifically, in a murine model, CMV airway infection and inhaled environmental antigen of poor intrinsic allergenic potential were found to sensitize for allergic airway disease (AAD) only when combined. Upon airway re-exposure to the inhaled antigen, Th-2 cells secrete interleukins (IL-4, IL-5, IL-9, and IL-25) known to induce goblet cell metaplasia, the lead histopathological manifestation of AAD that is characterized by thickening of airway epithelia and increased numbers of mucus-producing goblet cells, resulting in enhanced mucus secretion and airflow obstruction. As airway exposure to environmental antigens at the time of primary airway infection after hCMV transmission is a realistic scenario of medical interest, recent work modeled this scenario in the mouse with the aim to investigate a possible virus-allergen interplay [17] . Upon co-exposure of airway mucosa to inhaled antigen/low potency allergen, represented by OVA in the specific case, and mCMV, the virus activates MHC-II + CD11c + dendritic cells (DC) that localize to the mucosa, specifically DC of the CD11b + subset of conventional B220 low Ly6c low DC, briefly CD11b + cDC.	./cache/cord-304066-rirbdhz3.txt	./txt/cord-304066-rirbdhz3.txt