2016 Fiscal Year Final Research Report
The relationship between follicular helper T cells and pathogenesis of tonsillar hypertrophy in patients with child OSAS
| Project/Area Number |
15K20213
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Sapporo Medical University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HIMI Tetsuo 札幌医科大学, 医学部, 教授 (90181114)
ICHIMIYA Shingo 札幌医科大学, 医学部, 教授 (30305221)
KAMEKURA Ryuta 札幌医科大学, 医学部, 講師 (70404697)
NAGAYA Tomonori 札幌医科大学, 医学部, 助教 (60517902)
YAMASHITA Keiji 札幌医科大学, 医学部, 研究員 (50583580)
SHINTANI Tomoko とも耳鼻咽喉科, 院長 (10244352)
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| Research Collaborator |
Ito Fumie
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Keywords | 扁桃肥大 / 睡眠時無呼吸症候群 / アデノイド肥大 / 機能性リンパ球 / 濾胞ヘルパーＴ細胞 / 脂質メディエーター |
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| Outline of Final Research Achievements |
Obstructive sleep apnea syndrome (OSAS) in childhood is caused by adeno-tonsillar hypertrophy, and adeno-tonsillectomy is commonly performed as a treatment.Histologically, tonsillar hypertrophy is characterized by prominent germinal centers (GCs). Antigen specific humoral immune responses are established by the active interactions of B and Tfh cells (follicular helper T cells) in GCs. Therefore, we focused on the potential of these cells to induce lymphoid hyperplasia promoted in OSAS pathogenesis. The results revealed that the tonsils of OSAS were considerably different from those of RT tonsils in terms of Tfh cells. Moreover, lipoxin A4 and leukotriene B4 have the capacity to differentiate naive CD4+ T cells into Tfh cells. The results suggest that such lipid mediators have a potential role in the development of lymphoid follicles through the regulation of Tfh cell differentiation and regulation of these mediators should be considered as a candidate of conservative treatment.
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| Free Research Field |
耳鼻咽喉科
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