Abstract
Nasal hyperresponsiveness (NHR) is a characteristic feature of allergic rhinitis (AR); however, the pathogenesis of NHR is not fully understood. In this study, during the establishment of an experimental AR model using ovalbumin-immunized and -challenged mice, augmentation of the sneezing reaction in response to nonspecific proteins as well as a chemical stimulant was detected. Whether NHR is independent of mast cells and eosinophils was determined by using mast cell- and eosinophil-deficient mice. NHR was suppressed by treatment with anti-CD4 antibody, suggesting the pivotal contribution of CD4+ T cells. Furthermore, antigen challenge to mice to which in vitro-differentiated Th1, Th2, and Th17 cells but not naïve CD4+ T cells had been adoptively transferred led to the development of equivalent NHR. Since antigen-specific IgE and IgG were not produced in these mice and since antigen-specific IgE-transgenic mice did not develop NHR even upon antigen challenge, humoral immunity would be dispensable for NHR. CD4+ T cells play a crucial role in the pathogenesis of AR via induction of NHR, independent of IgE-, mast cell-, and eosinophil-mediated responses.
Highlights
Patients with allergic rhinitis (AR) develop several nasal symptoms including sneezing, rhinorrhea, and nasal congestion upon provocation with sensitized antigens
It is commonly considered that these symptoms are mediated by histamine and other chemical mediators derived from mast cells; IgE-mediated degranulation of these cells seems to have a crucial contribution to the induction of nasal responses [1,2]
Nasal hyperresponsiveness (NHR) was significantly detectable at 3 h after 4-time antigen challenge, peaked at 6 h, and disappeared by 48 h (Fig 1D)
Summary
Patients with allergic rhinitis (AR) develop several nasal symptoms including sneezing, rhinorrhea, and nasal congestion upon provocation with sensitized antigens. It is commonly considered that these symptoms are mediated by histamine and other chemical mediators derived from mast cells; IgE-mediated degranulation of these cells seems to have a crucial contribution to the induction of nasal responses [1,2]. AR is characterized by submucosal inflammation associated with massive accumulation of inflammatory cells including eosinophils and T cells, like other allergic diseases [1,3]. T Cell-Dependent Nasal Hyperresponsiveness collection and analysis, decision to publish, or preparation of the manuscript
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
