Roles of IL-17, Th1, and Tc1 cells in patients with IgG4-related sclerosing sialadenitis
Roles of IL-17, Th1, and Tc1 cells in patients with IgG4-related sclerosing sialadenitis
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DOI:
10.1002/lary.23429
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发表时间:
2012-10-01
期刊:
影响因子:
2.6
通讯作者:
Aoyagi, Masaru
中科院分区:
文献类型:
--
作者:
Ohta, Nobuo;Makihara, Seiichiro;Aoyagi, Masaru
Objectives/Hypothesis: Immunoglobulin G4 (IgG4)-related sclerosing sialadenitis is a recently recognized disease entity characterized by high serum IgG4 concentration and IgG4-producing plasma cell expansion in affected organs, which show fibrotic or sclerotic changes. However, little is known about the roles of CD4+ and CD8+ T cells or interleukin (IL)-17 in this disease. The purpose of this study was to evaluate the characteristics of CD4+ and CD8+ T cells and IL-17 in patients with IgG4-related sclerosing sialadenitis. Study Design: A retrospective clinical study at the Yamagata University School of Medicine. Methods: The patient group consisted of six males and four females with an average age of 57.9 years (range, 38 to 73years). Subsets of T helper (Th)1, Th2, T cytotoxic type (Tc)1, and Tc2 cells from patients with IgG4-related sclerosing sialadenitis were examined by using intracellular cytokine flow cytometry. Expression of IL-17 in the patients' lesions was also investigated immunohistochemically. Results: Six patients with IgG4-related sclerosing sialadenitis with high ratios of IgG4/IgG and prominent infiltration of IgG4-positive plasmacytes in the involved salivary glands had systemic complications, including pancreatitis, retroperitoneal fibrosis, and/or inflammatory pseudotumor of the lung after the initial swelling of the salivary glands. Populations of Th1 and Tc1 cells were significantly greater in IgG4-related sclerosing sialadenitis than in the controls (P < .05), but Th2 and Tc2 cell populations were not significantly increased. Expression of IL-17 was observed in the lesions of affected patients. Conclusions: Increases in Th1 and Tc1 cell populations and IL-17 expression might be involved in the mechanism of pathogenesis of IgG4-related sclerosing sialadenitis. Laryngoscope, 2012