Arachidonic acid metabolites-induced activation of group 2 innate lymphoid cell in eosinophilic upper airway inflammation

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  • Tojima Ichiro
    Department of Otorhinolaryngology, Shiga University of Medical Science
  • Shimizu Takeshi
    Department of Otorhinolaryngology, Shiga University of Medical Science

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  • 上気道の好酸球性炎症におけるアラキドン酸代謝物を介した2型自然リンパ球活性化機構

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Abstract

<p>Activated group 2 innate lymphoid cells (ILC2s) are important effector cells of Th2-type innate immune responses in eosinophilic airway inflammation by producing large amounts of Th2 cytokines such as IL-5, IL-13 and IL-4. Arachidonic acid metabolites including prostaglandins (PGs) and leukotrienes (LTs) play a vital role in homeostasis and inflammation. PGD2, LTB4, LTC4, LTD4, and LTE4 stimulate human ILC2s to produce Th2 cytokines. On the other hands, PGE2, PGI2 and lipoxin A4 inhibit Th2 cytokine productions from human ILC2s. Increasing evidences suggest that ILC2s are tissue-resident cells and their function and phenotype are influenced by the local microenvironment. Therefore, arachidonic acid metabolites in local mucosal tissues play very important roles in eosinophilic inflammation through tissue-resident ILC2s. ILC2s exist in both nasal polyp tissues in eosinophlic chronic rhinosinusitis (ECRS) and inferior nasal turbinate tissues in house dust mite (HDM)-induced allergic rhinitis. This review summarizes the association of tissue-resident ILC2s and arachidonic acid metabolites in nasal mucosa of ECRS and HDM-induced allergic rhinitis.</p>

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