Cytokine profiles contribute to understanding the pathogenic difference between good syndrome and oral lichen planus

takashi maehara, Masafumi Moriyama, Shintarou Kawano, Hayashida Jun-Nosuke, Sachiko Furukawa, Miho Ohta, Akihiko Tanaka, Masaki Yamauchi, Yukiko Ohyama, Tamotsu Kiyoshima, Seiji Nakamura

研究成果: ジャーナルへの寄稿記事

3 引用 (Scopus)

抄録

We described and analyzed the pathogenic difference between Good syndrome (GS) and oral lichen planus (OLP) in oral mucosa. Good syndrome (GS) is a rare disease characterized by B and T cell immunodeficiency associated with hypogammaglobulinemia and thymoma. GS patients frequently develop oral lichenoid lesions with lymphocytic infiltration beneath the basal layer. Oral lichen planus (OLP) is a chronic inflammatory disease of the oral mucosa characterized by destruction of basal cells by Langerhans cells, macrophages, and T lymphocytes. Although the histological features of the lesions of both diseases are very similar, the pathogenesis of GS in the oral mucosa remains unknown. In this study, we thus investigated the expression of infiltrating lymphocyte subsets (CD3, CD20, CD4, and CD8) and T helper (Th) cytokines including interferon (IFN)-γ (Th1 type), interleukin (IL)-4 (Th2 type), IL-17 (Th17 type), and IL-10 (regulatory T cell type) by immunohistochemistry in buccal mucosa specimens from 2 GS patients compared with 15 OLP patients. All patients showed a predominance of CD3 + T cells over CD20 + B cells, and CD4 + Th cells over CD8 + cytotoxic T cells. This polarization was especially prominent in GS. IFN-γ and IL-10 were strongly detected in the infiltrating lymphocytes of all patients. However, IL-4 and IL-17 were detected in OLP patients only. These results suggest that the pathogenesis of GS is different from that of OLP. GS is a unique inflammatory disorder characterized by dysfunction of Th2 and Th17 immune reactions via abnormal T-B cell interaction.

元の言語英語
ジャーナルMedicine (United States)
94
発行部数14
DOI
出版物ステータス出版済み - 4 6 2015

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Oral Lichen Planus
Cytokines
Mouth Mucosa
T-Lymphocytes
B-Lymphocytes
Interleukin-17
Interleukin-4
Interleukin-10
Interferons
Agammaglobulinemia
Thymoma
Langerhans Cells
Lymphocyte Subsets
Regulatory T-Lymphocytes
Rare Diseases
Helper-Inducer T-Lymphocytes
Cell Communication
Chronic Disease
Immunohistochemistry
Macrophages

All Science Journal Classification (ASJC) codes

  • Medicine(all)

これを引用

Cytokine profiles contribute to understanding the pathogenic difference between good syndrome and oral lichen planus. / maehara, takashi; Moriyama, Masafumi; Kawano, Shintarou; Jun-Nosuke, Hayashida; Furukawa, Sachiko; Ohta, Miho; Tanaka, Akihiko; Yamauchi, Masaki; Ohyama, Yukiko; Kiyoshima, Tamotsu; Nakamura, Seiji.

:: Medicine (United States), 巻 94, 番号 14, 06.04.2015.

研究成果: ジャーナルへの寄稿記事

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abstract = "We described and analyzed the pathogenic difference between Good syndrome (GS) and oral lichen planus (OLP) in oral mucosa. Good syndrome (GS) is a rare disease characterized by B and T cell immunodeficiency associated with hypogammaglobulinemia and thymoma. GS patients frequently develop oral lichenoid lesions with lymphocytic infiltration beneath the basal layer. Oral lichen planus (OLP) is a chronic inflammatory disease of the oral mucosa characterized by destruction of basal cells by Langerhans cells, macrophages, and T lymphocytes. Although the histological features of the lesions of both diseases are very similar, the pathogenesis of GS in the oral mucosa remains unknown. In this study, we thus investigated the expression of infiltrating lymphocyte subsets (CD3, CD20, CD4, and CD8) and T helper (Th) cytokines including interferon (IFN)-γ (Th1 type), interleukin (IL)-4 (Th2 type), IL-17 (Th17 type), and IL-10 (regulatory T cell type) by immunohistochemistry in buccal mucosa specimens from 2 GS patients compared with 15 OLP patients. All patients showed a predominance of CD3 + T cells over CD20 + B cells, and CD4 + Th cells over CD8 + cytotoxic T cells. This polarization was especially prominent in GS. IFN-γ and IL-10 were strongly detected in the infiltrating lymphocytes of all patients. However, IL-4 and IL-17 were detected in OLP patients only. These results suggest that the pathogenesis of GS is different from that of OLP. GS is a unique inflammatory disorder characterized by dysfunction of Th2 and Th17 immune reactions via abnormal T-B cell interaction.",
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AU - Jun-Nosuke, Hayashida

AU - Furukawa, Sachiko

AU - Ohta, Miho

AU - Tanaka, Akihiko

AU - Yamauchi, Masaki

AU - Ohyama, Yukiko

AU - Kiyoshima, Tamotsu

AU - Nakamura, Seiji

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AB - We described and analyzed the pathogenic difference between Good syndrome (GS) and oral lichen planus (OLP) in oral mucosa. Good syndrome (GS) is a rare disease characterized by B and T cell immunodeficiency associated with hypogammaglobulinemia and thymoma. GS patients frequently develop oral lichenoid lesions with lymphocytic infiltration beneath the basal layer. Oral lichen planus (OLP) is a chronic inflammatory disease of the oral mucosa characterized by destruction of basal cells by Langerhans cells, macrophages, and T lymphocytes. Although the histological features of the lesions of both diseases are very similar, the pathogenesis of GS in the oral mucosa remains unknown. In this study, we thus investigated the expression of infiltrating lymphocyte subsets (CD3, CD20, CD4, and CD8) and T helper (Th) cytokines including interferon (IFN)-γ (Th1 type), interleukin (IL)-4 (Th2 type), IL-17 (Th17 type), and IL-10 (regulatory T cell type) by immunohistochemistry in buccal mucosa specimens from 2 GS patients compared with 15 OLP patients. All patients showed a predominance of CD3 + T cells over CD20 + B cells, and CD4 + Th cells over CD8 + cytotoxic T cells. This polarization was especially prominent in GS. IFN-γ and IL-10 were strongly detected in the infiltrating lymphocytes of all patients. However, IL-4 and IL-17 were detected in OLP patients only. These results suggest that the pathogenesis of GS is different from that of OLP. GS is a unique inflammatory disorder characterized by dysfunction of Th2 and Th17 immune reactions via abnormal T-B cell interaction.

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