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

Ryuta Kamekura | Zendy; Kenichi Takano | Zendy; Motohisa Yamamoto | Zendy; Koji Kawata | Zendy; Katsunori Shigehara | Zendy; Sumito Jitsukawa | Zendy; Tomonori Nagaya | Zendy; Fumie Ito | Zendy; Akinori Sato | Zendy; Noriko Ogasawara | Zendy; Chieko Tsubomatsu | Zendy; Hiroki Takahashi | Zendy; Hiroshi Nakase | Zendy; Tetsuo Himi | Zendy; Shingo Ichimiya | Zendy

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

Author(s) -

Ryuta Kamekura,

Kenichi Takano,

Motohisa Yamamoto,

Koji Kawata,

Katsunori Shigehara,

Sumito Jitsukawa,

Tomonori Nagaya,

Fumie Ito,

Akinori Sato,

Noriko Ogasawara,

Chieko Tsubomatsu,

Hiroki Takahashi,

Hiroshi Nakase,

Tetsuo Himi,

Shingo Ichimiya

Publication year - 2017

Publication title -

the journal of immunology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.737

H-Index - 372

eISSN - 1550-6606

pISSN - 0022-1767

DOI - 10.4049/jimmunol.1601507

Subject(s) - pathogenesis , sialadenitis , igg4 related disease , infiltration (hvac) , immunology , germinal center , disease , medicine , b cell , lymphoma , follicular phase , pathology , follicular lymphoma , dacryoadenitis , biology , antibody , salivary gland , physics , thermodynamics

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.

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