Allergic rhinitis, the usual suspects
Reviewed by Hassan Mohammed

Allergic rhinitis (AR) is characterised by allergen binding to IgE on mast cells and basophils and subsequent histamine, prostaglandine D2 (PGD2) and cysteinyl leukotrienes (cysLTs) release causing early-phase response. This is followed by late-phase response mediated by eosinophils. Other cells, Group 2 innate lymphoid cells (ILC2s), respond to inflammatory factors released from airway cells as a result of exposure to allergens. ILC2s release Th2 cytokines, ILs 5,9,13 and amphiregulin with subsequent airway eosinophilia. This study investigates the prevalence and activating mechanisms of ILC2s in the inferior nasal turbinate (INT) tissues of AR and non-AR subjects: 18 patients with house dust mite induced AR and 13 controls. AR was diagnosed by the nasal provocation test (NPT), skin prick test and RAST test. Biopsies from inferior turbinates were taken at surgery and nasal lavage (NL) was performed after NPT. In AR patients, ILC2 prevalence was significantly more than that in controls. Also, following NPT, PGD2 and CysLTs levels increase in NL. In culture, PGD2 and CycLTs induced IL5 and 13 production from ILC2s. IL13 production was inhibited by montelukast, a CysLT1 antagonist. Authors concluded that PGD2 and cysLTs may activate ILC2s to produce Th2 cytokines, IL 5 and 13, leading to allergic inflammation in AR. The findings of this study bring us one step closer to understanding AR. However, the sample is small, the standard deviation appears to be large when ILC2 prevalence is measured and also, PGD2 and CysLTs increased in NL of only four subjects of AR patients.

Evidence for the induction of Th2 inflammation by group 2 innate lymphoid cells in response to prostaglandin D2 and cysteinyl leukotrienes in allergic rhinitis.
Tojima I, Matsumoto K, Kikuoka H, et al.
ALLERGY
2019;74:2417-26.