Abstract
Allergic asthma involves a complex series of reactions within the airways that lead to inflammation and bronchoconstriction. These phenomena are closely linked to the immune response to the allergenic protein mediated by T cells with specificity for the allergen. Antigen presentation by dendritic cells initiates the allergic response, triggering the activation of CD4+ T cells predominantly. These cells secrete Th2 type cytokines, of which IL-4 and IL-5 are best understood, that act on various cells including B cells, eosinophils, macrophages and epithelial cells. These cells mediate, in turn, immunoglobulin E synthesis, and promote an eosinophil rich inflammation through the concerted action of various chemoattractant substances, both lipid-derived and proteins. CD8+ T cells are also activated and may have either anti-inflammatory or pro-inflammatory effects, depending upon the particular experimental model studied. The T cell receptor (TCR) that these cells possess has an important influence on the role they play. TCRalphabeta cells appear more likely to be pro-inflammatory and have antigen specificity whereas TCRgammadelta cells can be either pro- or anti-inflammatory, depending on species and experimental conditions and are not antigen specific. In conclusion, the magnitudes of inflammatory responses and bronchoconstriction following allergen challenge of sensitised animals are T cell driven and are determined, at least in part, by the balance of the T cell subsets that are activated.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: 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.