{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T19:02:34Z","timestamp":1790622154645,"version":"4.1.0"},"reference-count":51,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,8,12]],"date-time":"2019-08-12T00:00:00Z","timestamp":1565568000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000646","name":"Japan Society for the Promotion of Science London","doi-asserted-by":"publisher","award":["26861371"],"award-info":[{"award-number":["26861371"]}],"id":[{"id":"10.13039\/501100000646","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005620","name":"North Carolina GlaxoSmithKline Foundation","doi-asserted-by":"publisher","award":["2504"],"award-info":[{"award-number":["2504"]}],"id":[{"id":"10.13039\/100005620","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Allergy"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Group 2 innate lymphoid cells (ILC2s) play important roles in allergic inflammation. However, their roles in the pathophysiology of allergic rhinitis (AR) are poorly understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>Prevalence of ILC2s in the inferior nasal turbinate (INT) tissues and the activating mechanisms of ILC2s were examined in patients with house dust mite (HDM)\u2010induced AR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Eighteen patients with HDM\u2010induced AR and 13 control subjects were recruited. Fresh INT tissues and peripheral blood mononuclear cells (PBMCs) were analysed using flow cytometry. Nasal lavage fluids (NLF) were collected at 10\u00a0minutes after the nasal provocation test (NPT) with HDM disc, and released mediators were measured by ELISA. Sorted ILC2s were cultured and stimulated with mediators associated with AR.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The prevalence of ILC2s was significantly increased in nasal mucosa of patients with HDM\u2010induced AR, and it was positively correlated with the number of infiltrating eosinophils. ILC2s in the INT tissues expressed a prostaglandin D\n                      <jats:sub>2<\/jats:sub>\n                      (PGD\n                      <jats:sub>2<\/jats:sub>\n                      ) receptor, chemoattractant receptor\u2010homologous molecule\u2010expressed TH2 cells (CRTH2) and a cysteinyl leukotriene (cysLTs) receptor, CysLT1. After NPT, the number of eosinophils and concentrations of PGD\n                      <jats:sub>2<\/jats:sub>\n                      and cysLTs were significantly increased in the NLF from AR patients. PGD\n                      <jats:sub>2<\/jats:sub>\n                      and cysLTs significantly induced IL\u20105 production from cultured PBMC\u2010derived ILC2s dose\u2010dependently. PGD\n                      <jats:sub>2<\/jats:sub>\n                      \u2010induced and cysLTs\u2010induced productions of IL\u20105 and IL\u201013 from ILC2s were completely inhibited by ramatroban, a dual CRTH2 and thromboxane receptor antagonist, and montelukast, a CysLT1 antagonist, respectively.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      PGD\n                      <jats:sub>2<\/jats:sub>\n                      \u2010CRTH2 and cysLTs\u2010CysLT1 axes may activate tissue\u2010resident ILC2s to produce Th2 cytokines, IL\u20105 and IL\u201013, leading to the development of allergic inflammation in AR.\n                    <\/jats:p>\n                  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