Complement C3a Regulates Muc5ac Expression by Airway Clara Cells Independent of TH2 Responses
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چکیده
Independent of TH2 Responses Patricia Dillard, Rick A. Wetsel, and Scott M. Drouin The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases and Department of Biochemistry and Molecular Biology, The University of Texas Health Science Center at Houston, Houston, TX 77030 USA Correspondence and reprint requests should be addressed to Scott M. Drouin, Ph.D., The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, The University of Texas Health Science Center at Houston, 1825 Pressler St, Houston, TX 77030 USA Corresponding Author: Scott M. Drouin Phone: (713) 500-2446 Fax: (713) 500-2424 Email: [email protected] Supported by National Institutes of Health Grants AI025011 and HL074333 (to R.A.W.) and K22 AI52407 (to S.M.D.). Running Title: Regulation of Clara Cell Muc5ac Expression by C3a Descriptor Number: 61 Word Count: 4571 AJRCCM Articles in Press. Published on March 30, 2007 as doi:10.1164/rccm.200701-049OC
منابع مشابه
Complement C3a regulates Muc5ac expression by airway Clara cells independently of Th2 responses.
RATIONALE The factors that control the secretion of epithelial mucins are essential to understanding obstructive airway diseases such as asthma. Although the complement anaphylatoxin C3a and its receptor have been shown to promote many features of allergic lung inflammation, the contribution to mucin expression has not been elucidated. OBJECTIVES To determine if the C3a receptor with its liga...
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The complement system forms the central core of innate immunity but also mediates a variety of inflammatory responses. Anaphylatoxin C3a, which is generated as a byproduct of complement activation, has long been known to activate mast cells, basophils and eosinophils and to cause smooth muscle contraction. However, the role of C3a in the pathogenesis of allergic asthma remains unclear. In this ...
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تاریخ انتشار 2007