Cutting Edge: A Critical Role of Lesional T Follicular Helper Cells in the Pathogenesis of IgG4-Related Disease

被引:65
作者
Kamekura, Ryuta [1 ,2 ]
Takano, Kenichi [2 ]
Yamamoto, Motohisa [3 ]
Kawata, Koji [1 ]
Shigehara, Katsunori [1 ]
Jitsukawa, Sumito [1 ,2 ]
Nagaya, Tomonori [2 ]
Ito, Fumie [1 ,2 ]
Sato, Akinori [1 ]
Ogasawara, Noriko [2 ]
Tsubomatsu, Chieko [2 ]
Takahashi, Hiroki [3 ]
Nakase, Hiroshi [4 ]
Himi, Tetsuo [2 ]
Ichimiya, Shingo [1 ]
机构
[1] Sapporo Med Univ, Sch Med, Res Inst Frontier Med, Dept Human Immunol,Chuo Ku, South 1,West 17, Sapporo, Hokkaido 0608556, Japan
[2] Sapporo Med Univ, Sch Med, Dept Otolaryngol, Chuo Ku, Sapporo, Hokkaido 0608543, Japan
[3] Sapporo Med Univ, Sch Med, Dept Rheumatol, Chuo Ku, Sapporo, Hokkaido 0608543, Japan
[4] Sapporo Med Univ, Sch Med, Dept Gastroenterol & Hepatol, Chuo Ku, Sapporo, Hokkaido 0608543, Japan
关键词
DACRYOADENITIS; CRITERIA; IGG4;
D O I
10.4049/jimmunol.1601507
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
IgG4-related disease (IgG4-RD) is a newly recognized systemic chronic fibroinflammatory disease. However, the pathogenesis of IgG4-RD remains unknown. To determine the pathophysiologic features of IgG4-RD, we examined T follicular helper (Tfh) cells in lesions and blood from patients with IgG4-RD. Patients with IgG4-related dacryoadenitis and sialadenitis (IgG4-DS) showed increased infiltration of Tfh cells highly expressing programmed death 1 and ICOS in submandibular glands. Tfh cells from IgG4-DS submandibular glands had higher expression of B cell lymphoma 6 and a greater capacity to help B cells produce IgG4 than did tonsillar Tfh cells. We also found that the percentage of programmed death 1 hi circulating Tfh cells in IgG4-DS patients was higher than that in healthy volunteers and was well correlated with clinical parameters. Our findings indicate that anomalous Tfh cells in tissue lesions of IgG4-RD have features distinct from those in lymphoid counterparts or blood and potentially regulate local IgG4 production in IgG4-RD.
引用
收藏
页码:2624 / 2629
页数:6
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