Autoimmune Responses and Immune Mediators Induced by Cytosolic DNA Fragments in Graves’ Disease | Chapter 5 | Current Innovations in Medicine and Medical Science Vol. 5

 Graves ’ hyperthyroidism is caused by autoantibodies against the thyroid- stimulating hormone receptor( TSHR) that mimic the action of thyroid- stimulating hormone. The establishment of Graves ’ hyperthyroidism in experimental creatures is an important approach for probing the mechanisms of tone- forbearance breakdown that lead to the product of thyroid- stimulating TSHR autoantibodies. Shimojo’s model was the first successful Graves ’ beast model, generated using AKR/ N( H- 2k) mice. This model highlights the significance of coincident major histocompatibility complex( MHC) class II expression in TSHR- expressing cells in the development of Graves ’ hyperthyroidism. We set up that cytosolic tone- genomic DNA fractions attained from sterile injured cells can induce abnormal MHC class II expression as well as the product of multitudinous seditious cytokines and chemokines in thyrocytes in vitro, inferring that severe cell injury can initiate vulnerable responses related to thyroid autoimmunity and intermediated by cytosolic DNA signalling. In vivo and in vitro studies suggest that induction of antigen- processing and- presenting genes, including MHC motes, could be elicited, at least in part, by the type I interferon( IFN) or IFN- γ signaling pathway. likewise, successful Graves ’ beast models have been established primarily by immunizing mice with TSHR- expressing plasmids or adenoviruses. In these models, double- stranded DNA vaccines presumably ply analogous vulnerable- cranking goods in cells at the inoculation point. This chapter focuses on substantiation suggesting that cell injury- deduced tone- DNA fractions act as a detector of Graves ’ complaint and discusses the implicit molecular mechanisms by which cytosolic dsDNA can induce MHC motes.

Author(s) Details:

Yoko Fujiwara,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Kaga-2-11-1, Itabashi, Tokyo-173-8605, Japan.

Yuqian Luo,
Department of Laboratory Medicine, Nanjing Drum Tower Hospital, Nanjing University Medical School, Nanjing, China.

Mitsuo Kiriya,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Kaga-2-11-1, Itabashi, Tokyo-173-8605, Japan.

Akira Kawashima,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Kaga-2-11-1, Itabashi, Tokyo-173-8605, Japan.

Aya Yoshihara,
Department of Education Planning and Development, Faculty of Medicine, Toho University, 5-21-16 Omorinishi, Ota, Tokyo-143-8540, Japan.

Kazunari Tanigawa,
Department of Molecular Pharmaceutics, Faculty of Pharma-Science Teikyo University, Itabashi-ku, Tokyo-173-8605, Japan.

Yasuhiro Nakamura,
Center for Promotion of Pharmaceutical Education & Research, Faculty of Pharma-Science, Teikyo University, Tokyo-173-8605, Japan

Keiji Maruyama,
Center for Promotion of Pharmaceutical Education & Research, Faculty of Pharma-Science, Teikyo University, Tokyo-173-8605, Japan

Shigekazu Watanabe,
Center for Promotion of Pharmaceutical Education & Research, Faculty of Pharma-Science, Teikyo University, Tokyo-173-8605, Japan

Koichi Suzuki,
Department of Clinical Laboratory Science, Faculty of Medical Technology, Teikyo University, Kaga-2-11-1, Itabashi, Tokyo-173-8605, Japan.

Please see the link here: https://stm.bookpi.org/CIMMS-V5/article/view/8462