Journal
FRONTIERS IN IMMUNOLOGY
Volume 12, Issue -, Pages -Publisher
FRONTIERS MEDIA SA
DOI: 10.3389/fimmu.2021.663626
Keywords
allergic rhinitis; tight junction; TSLP; IL-25; IL-33; innate lymphoid cells; Th2 cytokines; epigenetic
Categories
Funding
- Universiti Sains Malaysia (USM) [1001/PPSP/8012349, 1001.PPSP.8012285]
- USM Fellowship Scheme
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Allergic rhinitis is a common disorder affecting up to 40% of the global population, characterized by impaired nasal epithelial barrier and crucial involvement of TJ molecules in its pathogenesis. Various regulatory factors have been identified, offering hope for the development of novel therapeutic approaches.
Allergic rhinitis (AR) is a common disorder affecting up to 40% of the population worldwide and it usually persists throughout life. Nasal epithelial barrier constitutes the first line of defense against invasion of harmful pathogens or aeroallergens. Cell junctions comprising of tight junctions (TJs), adherens junctions, desmosomes and hemidesmosomes form the nasal epithelial barrier. Impairment of TJ molecules plays causative roles in the pathogenesis of AR. In this review, we describe and discuss the components of TJs and their disruption leading to development of AR, as well as regulation of TJs expression by epigenetic changes, neuro-immune interaction, epithelial-derived cytokines (thymic stromal lymphopoietin, IL-25 and IL-33), T helper 2 (Th2) cytokines (IL-4, IL-5, IL-6 and IL-13) and innate lymphoid cells. These growing evidence support the development of novel therapeutic approaches to restore nasal epithelial TJs expression in AR patients.
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