U.S. flagAn official website of the United States government
                    Here's how you know **Official websites use .gov**
                            
                            A **.gov** website belongs to an official government organization in the United States.
 **Secure .gov websites use HTTPS**
                            
                            A **lock** (                            
                              A locked padlock                                                      
                            
                            ) or **https://** means you’ve safely connected to the .gov website. Share sensitive information only on official, secure websites.


Menu Agricultural Research Service
						
                    U.S. DEPARTMENT OF AGRICULTURE
 Animal Parasitic Diseases Laboratory: Beltsville, MD
 close



    Research

                    Research Projects
                                    Publications
                                    Collaborations
                                    News
                People

                    Staff Listing
                                    Careers


        


                    Resources
                        Our ScientistsSearch small
                    Search
            
            ARS Home
                                About ARS
                                Contact Us




ARS Home Northeast Area Beltsville, Maryland (BARC) Beltsville Agricultural Research Center Animal Parasitic Diseases Laboratory Research Publications at this Location





- ARS National Programs
- Search for a scientific manuscript
- Search for a research project
- ARS Software
- Programs and Projects
- Collaborations
- Subjects of Investigation
- Publications

Title:   Author  item
                                            PALANIYANDI, SENTHILKUMAR - University Of Marylanditem
                                            LIU, XIAOYANG - University Of Marylanditem
                                            PERIYASAMY, SIVAKUMAR - Albany Medical Collegeitem
                                            MA, AIYING - University Of Marylanditem
                                            Jenkins, Markitem
                                            Tuo, Wenbinitem
                                            SONG, WENXIA - University Of Marylanditem
                                            KEEGAN, ACHSAH - University Of Marylanditem
                                            CONRAD, DANIEL - Virginia Commonwealth Universityitem
                                            ZHU, XIAOPING - University Of Maryland
  Submitted to: Mucosal Immunology
                                    Publication Type: Peer Reviewed Journal
                                    Publication Acceptance Date: 3/1/2015
                                    Publication  Date: 3/18/2015
                                    Citation: Palaniyandi, S., Liu, X., Periyasamy, S., Ma, A., Jenkins, M.C., Tuo, W., Song, W., Keegan, A.D., Conrad, D.H., Zhu, X. 2015. Inhibition of CD23-mediated IgE transcytosis suppresses the  initiation and development of airway allergic inflammation. Mucosal Immunology. DOI:10.1038/mi.2015.16.Interpretive Summary: Inflammatory responses to airborne allergens are controlled by epithelial cells lining the lung and airway.  Better understanding the receptors that mediate transport of allergens might provide new ways to ameliorate asthma and allergic responses to airborne irritants, including lungworms and other respiratory pathogens of livestock.  Here we investigated, in mice, how a particular cell surface receptor (CD23) plays a role in transporting allergens, bound by immunoglobulin E (IgE), across the lining of the airway.  Mice lacking this receptor in epithelia lining the airway did not mount inflammatory responses when exposed to allergens, but did when supplemented with bone marrow donated from normal mice.  Having such receptors elsewhere in the body did not lead to inflammatory responses, underscoring the requirement for this receptor on epithelial cells lining the airway. Inflammation could be suppressed by administering antibodies to this receptor. Taken together, the present study identified a mechanism where epithelial CD23 mediates respiratory inflammation. Blocking CD23 may be a therapeutic method to prevent or ameliorate asthma. These results may interest immunologists, veterinarians, and the pharmaceutical industry, and others interested in infectious and non-infectious induced respiratory disease.
                                Technical Abstract: The epithelium lining the airway tract and allergen-specific IgE are considered essential controllers of inflammatory responses to allergens. The human IgE receptor, CD23 (Fc'RII), is capable of transporting IgE or IgE-allergen complexes across the polarized human airway epithelial cell (AEC) monolayer in vitro. However, it remains completely unknown whether CD23-dependent IgE transfer pathway in AECs initiates and facilitates allergic inflammation in
vivo and whether the inhibition of such a pathway can attenuate the allergic inflammation. To prove this, we first showed that epithelial CD23 in wild-type (WT) mice transcytosed either IgE
or ovalbumin (OVA)-IgE complexes across the airway epithelial barrier. Neither type of transcytosis was observed in CD23-knockout (KO) mice. The OVA sensitization and aerosol challenge of the irradiated bone-marrow chimeric mice (WT/WT) that CD23 expressed on radioresistant airway structural cells, mainly in epithelial cells, resulted in airway eosinophilia, lung damages including collagen deposition and significantly increased goblet cells, and increased airways hyperreactivity. In contrast, the absence of CD23 expression on airway structural or epithelial cells, but not on hematopoietic cells, of the chimeric mice (WT/CD23KO) significantly reduced OVA-driven allergic airway inflammation. Finally, inhalation of a CD23-blocking B3B4 antibody to target exposed CD23 in AECs of the sensitized WT mice before or during airway challenge suppressed the salient features of asthma, including bronchial hyperreactivity. Taken together, these results identify a previously unproven mechanism in which, epithelial CD23 plays a central role in the development of allergic inflammation in vivo. Our study further suggests that the functional inhibition of CD23 on AECs is a potential therapeutic means to intervene the asthma development.


Return to top


Connect with ARS Sign up


ARS Home
                            USDA.gov
                            Plain Writing
                            Policies & Links
                            Civil Rights Statements
                            FOIA
                            Accessibility Statement
                            Privacy Policy
                            Non-Discrimination Statement
                            Quality of Information
                            USA.gov
                            WhiteHouse.gov