Crucial Role of Tissue-specific Apoptosis on the Development of Primary Sjögren's Syndrome

DOI
  • Hayashi Yoshio
    Department of Oral Molecular Pathology, Institute of Health Bioscience, The University of Tokushima Graduate School
  • Arakaki Rieko
    Department of Oral Molecular Pathology, Institute of Health Bioscience, The University of Tokushima Graduate School
  • Ishimaru Naozumi
    Department of Oral Molecular Pathology, Institute of Health Bioscience, The University of Tokushima Graduate School

書誌事項

公開日
2004
DOI
  • 10.11277/osi.1.55
公開者
特定非営利活動法人　日本口腔科学会

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説明

Primary Sjögren's syndrome is an autoimmune disorder characterized by lymphocytic infiltrates and destruction of the salivary and lacrimal glands, and systemic production of autoantibodies to the ribonucleoprotein (RNP) particles SS-A/Ro and SS-B/La, leading to clinical symptoms of dryness of the mouth and eyes (sicca syndrome). Autoreactive T cells bearing the CD4 molecule may recognize an unknown self antigen, triggering autoimmunity in the salivary and lacrimal glands. Although several candidate autoantigens including α-fodrin have been reported in Sjögren's syndrome, the pathogenic roles of the autoantigens in initiation and progression of SS are still unclear. It is possible that individual T cells activated by an appropriate self antigen can proliferate and form a restricted clone. Recent evidence suggests that the apoptotic pathway plays a central role in making T cells tolerant to tissue-specific self antigen, and may drive the autoimmune phenomenon. We recently reported that tissue-specific apoptosis in estrogen-deficient mice may contribute to autoantigen cleavage, leading to the development of autoimmune exocrinopathy. The studies reviewed imply that tissue-specific apoptosis and caspase-mediated α-fodrin proteolysis are involved in the progression of autoimmune lesions in Sjögren's syndrome. Moreover, Fas ligand (FasL) and its receptor Fas are essential in the homeostasis of the peripheral immune system. It is considered that a defect in activation-induced cell death (AICD) of effector T cells may result in the development of autoimmune exocrinopathy in Sjögren's syndrome.

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詳細情報 詳細情報について

  • CRID
    1390001205221196544
  • NII論文ID
    130004503798
  • DOI
    10.11277/osi.1.55
  • ISSN
    18814204
    13488643
  • 本文言語コード
    en
  • データソース種別
    • JaLC
    • CiNii Articles
  • 抄録ライセンスフラグ
    使用不可

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