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大学・研究所にある論文を検索できる 「Increased blood group 2 innate lymphoid cells are associated with the clinical severity of Kimura disease.」の論文概要。リケラボ論文検索は、全国の大学リポジトリにある学位論文・教授論文を一括検索できる論文検索サービスです。

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Increased blood group 2 innate lymphoid cells are associated with the clinical severity of Kimura disease.

TOJIMA Ichiro 80567347 0000-0001-7687-9427 MURAO Takuya NAKAMURA Keigo 50848380 0000-0003-2570-9529 ARAI Hiroyuki 60816627 0000-0002-9120-3035 MATSUMOTO Koji 0000-0001-8839-3440 SHIMIZU Shino 50505592 0000-0002-0704-9048 KOUZAKI Hideaki 10402710 0000-0001-5460-4967 SHIMIZU Takeshi 00206202 0000-0002-1344-7210 滋賀医科大学

2022.10.22

概要

Dear Editor,
Kimura disease (KD) is a chronic inflammatory disorder characterized by general itching, subcutaneous head and neck mass lesions with tissue eosinophilia, blood eosinophilia, and elevated serum IgE levels.1 KD is a rare disorder, and only 238 cases have been reported worldwide in the last 30 years.2 Although the mass lesions are eradicated by surgery and steroid therapy, the disease frequently recurs. The precise etiology of this disease is unknown. Several researchers have reported the role of type 2 cytokines in the pathogenesis of KD; interleukin (IL) -4- and IL-5-expressing mast cells and T cells accumulate in local lesions,3 and the mRNA expressions encoding IL-4, IL-5, and IL-13 in peripheral blood mononuclear cells (PBMCs) were positively correlated with the number of blood eosinophils.4

Group 2 innate lymphoid cells (ILC2s) have been identified as important effector cells for eosinophilic airway inflammation such as allergic rhinitis (AR), chronic rhinosinusitis, and asthma.5 ILC2s in mucosal tissues play critical roles in the induction of type 2 inflammation through the production of IL-4, IL-5, and IL-13 in response to various mediators such as prostaglandin (PG) D2 and leukotriene (LT) C4, D4, and E45 released by eosinophils and mast cells.6,7 However, the role of blood ILC2s in eosinophilic inflammation, such as KD, has not been well understood. We examined the prevalence of blood ILC2s; their ability to produce IL-4, IL-5, IL-13, and IL-31; and serum concentrations of these type 2 cytokines in patients with KD compared with those in patients with HDM-induced AR and control subjects (Supplementary Methods).

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参考文献

1. Chen H, Thompson LD, Aguilera NS, Abbondanzo SL. Kimura disease: a clinico- pathologic study of 21 cases. Am J Surg Pathol 2004;28:505e13.

2. Kakehi E, Kotani K, Otsuka Y, Fukuyasu Y, Hashimoto Y, Sakurai S, et al. Kimu- ra's disease: effects of age on clinical presentation. QJM 2020;113:336e45.

3. Kimura Y, Pawankar R, Aoki M, Niimi Y, Kawana S. Mast cells and T cells in Kimura's disease express increased levels of interleukin-4, interleukin-5, eotaxin and RANTES. Clin Exp Allergy 2002;32:1787e93.

4. Katagiri K, Itami S, Hatano Y, Yamaguchi T, Takayasu S. In vivo expression of IL- 4, IL-5, IL-13 and IFN-gamma mRNAs in peripheral blood mononuclear cells and effect of cyclosporine A in a patient with Kimura's disease. Br J Dermatol 1997;137:972e7.

5. Kato A. Group 2 innate lymphoid cells in airway diseases. Chest 2019;156: 141e9.

6. Miyata J, Fukunaga K, Kawashima Y, Ohara O, Arita M. Cysteinyl leukotriene metabolism of human eosinophils in allergic disease. Allergol Int 2020;69: 28e34.

7. Luna-Gomes T, Magalh~aes KG, Mesquita-Santos FP, Bakker-Abreu I, Samico RF, Molinaro R, et al. Eosinophils as a novel cell source of prostaglandin D2: auto- crine role in allergic inflammation. J Immunol 2011;187:6518e26.

8. Oejen LK, Mack MR, Feng J, Whelan TM, Niu H, Guo CJ, et al. Sensory neurons co-opt classical immune signaling pathways to mediate chronic itch. Cell 2017;171:217e28.

9. Nakashima C, Otsuka A, Kabashima K. Interleukin-31 and interleukin-31 recep- tor: new therapeutic targets for atopic dermatitis. Exp Dermatol 2018;27: 327e31.

10. Lai T, Wu D, Li W, Chen M, Yi Z, Huang D, et al. Interleukin-31 expression and relation to disease severity in human asthma. Sci Rep 2016;6:22835.

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