delayed goblet cell hyperplasia, acetylcholine receptor expression, and worm expulsion in smc-specific il-4rα–deficient mice延迟杯状细胞增生、乙酰胆碱受体表达和蠕虫驱逐在smc-specific il-4rα-deficient老鼠.pdfVIP

delayed goblet cell hyperplasia, acetylcholine receptor expression, and worm expulsion in smc-specific il-4rα–deficient mice延迟杯状细胞增生、乙酰胆碱受体表达和蠕虫驱逐在smc-specific il-4rα-deficient老鼠.pdf

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delayed goblet cell hyperplasia, acetylcholine receptor expression, and worm expulsion in smc-specific il-4rα–deficient mice延迟杯状细胞增生、乙酰胆碱受体表达和蠕虫驱逐在smc-specific il-4rα-deficient老鼠

Delayed Goblet Cell Hyperplasia, Acetylcholine Receptor Expression, and Worm Expulsion in SMC-Specific IL-4Ra–Deficient Mice 1 1 1 1 1 1 William G. C. Horsnell , Antony J. Cutler , Claire J. Hoving , Helen Mearns , Elmarie Myburgh , Berenice Arendse , 2 3 4 1* Fred D. Finkelman , Gary K. Owens , Dave Erle , Frank Brombacher 1 Division of Immunology, Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, Cape Town, South Africa, 2 Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, Ohio, United States of America, 3 Department of Molecular Physiology and Biological Physics, University of Virginia Health Sciences Center, Charlottesville, Virginia, United States of America, 4 Lung Biology Center, Department of Medicine, University of California San Francisco, San Francisco, California, United States of America Interleukin 4 receptor a (IL-4Ra) is essential for effective clearance of gastrointestinal nematode infections. Smooth muscle cells are considered to play a role in the type 2 immune response–driven expulsion of gastrointestinal nematodes. Previous studies have shown in vitro that signal transducer and activator of transcription 6 signaling in response to parasitic nematode infection significantly increases smooth muscle cell contractility. Inhibition of the IL- 4Ra pathway inhibits this response. How this response manifests itself in vivo is unknown. In this study, smooth muscle cell IL-4Ra–deficient mice (SM-MHCCreIL-4Ra/lox) were generated and characterized to uncover any role for IL-4/IL-13 in this non–immune cell type in response to

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