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- Heike Toshio
- Department of Physiology, Keio University School of Medicine
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- Saito Megumu K
- Clinical Application Department, Center for iPS cell research and application, Kyoto University
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- Nishikomori Ryuta
- Department of Physiology, Keio University School of Medicine
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- Yasumi Takahiro
- Department of Physiology, Keio University School of Medicine
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- Nakahata Tatsutoshi
- Clinical Application Department, Center for iPS cell research and application, Kyoto University
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抄録
The autoinflammatory diseases are characterized by seemingly unprovoked episodes of inflammation, without high-titer autoantibodies or antigen-specific T cells. The concept was proposed ten years ago with the identification of the genes underlying hereditary periodic fever syndromes. NLRP3 inflammasome activation and IL-1β secretion have recently emerged as a central mechanism in the pathogenesis of disease. Here we describe four genetically defined syndromes like cryopyrin-associated periodic syndromes (CAPS, cryopyrinopathies), mevalonate kinase deficiency (MKD) or hyper-IgD and periodic fever syndrome (HIDS), pyogenic aseptic arthritis, pyoderma gangrenosum, and acne syndrome (PAPA syndrome), and deficiency of interleukin-1-receptor antagonist (DIRA) along with the pitfall for understanding the pathphysiology.
収録刊行物
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- Inflammation and Regeneration
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Inflammation and Regeneration 31 (2), 125-136, 2011
一般社団法人 日本炎症・再生医学会
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詳細情報 詳細情報について
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- CRID
- 1390282680235007872
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- NII論文ID
- 130004943778
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- ISSN
- 18808190
- 18809693
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- 本文言語コード
- en
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- データソース種別
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- JaLC
- Crossref
- CiNii Articles
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- 抄録ライセンスフラグ
- 使用不可