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- 저자 : Kiyoshi Takeda (검색결과 6 건)
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Host–microbiota interactions in rheumatoid arthritis
Yuichi Maeda,Kiyoshi Takeda 생화학분자생물학회 2019 Experimental and molecular medicine Vol.51 No.-
The gut microbiota has been proposed to be an important environmental factor in the development of rheumatoid arthritis (RA). Here, we review a growing body of evidence from human and animal studies that supports the hypothesis that intestinal microbiota play a role in RA. Previous studies from we and others showed an altered composition of the microbiota in early RA patients. A recent study demonstrated that Prevotella species are dominant in the intestine of patients in the preclinical stages of RA. In addition, Prevotella-dominated microbiota isolated from RA patients contributes to the development of Th17 cell-dependent arthritis in SKG mice. Moreover, it was reported that periodontal bacteria correlates with the pathogenesis of RA. In this review, we discuss the link between oral bacteria and the development of arthritis. However, many questions remain to be elucidated in terms of molecular mechanisms for the involvement of intestinal and oral microbiota in RA pathogenesis.
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Roles of intestinal epithelial cells in the maintenance of gut homeostasis
Ryu Okumura,Kiyoshi Takeda 생화학분자생물학회 2017 Experimental and molecular medicine Vol.49 No.-
The intestine is a unique organ inhabited by a tremendous number of microorganisms. Intestinal epithelial cells greatly contribute to the maintenance of the symbiotic relationship between gut microbiota and the host by constructing mucosal barriers, secreting various immunological mediators and delivering bacterial antigens. Mucosal barriers, including physical barriers and chemical barriers, spatially segregate gut microbiota and the host immune system to avoid unnecessary immune responses to gut microbes, leading to the intestinal inflammation. In addition, various immunological mediators, including cytokines and chemokines, secreted from intestinal epithelial cells stimulated by gut microbiota modulate host immune responses, maintaining a well-balanced relationship between gut microbes and the host immune system. Therefore, impairment of the innate immune functions of intestinal epithelial cells is associated with intestinal inflammation.
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Regulation of Intestinal Homeostasis by Innate Immune Cells
Kayama, Hisako,Nishimura, Junichi,Takeda, Kiyoshi The Korean Association of Immunobiologists 2013 Immune Network Vol.13 No.6
The intestinal immune system has an ability to distinguish between the microbiota and pathogenic bacteria, and then activate pro-inflammatory pathways against pathogens for host defense while remaining unresponsive to the microbiota and dietary antigens. In the intestine, abnormal activation of innate immunity causes development of several inflammatory disorders such as inflammatory bowel diseases (IBD). Thus, activity of innate immunity is finely regulated in the intestine. To date, multiple innate immune cells have been shown to maintain gut homeostasis by preventing inadequate adaptive immune responses in the murine intestine. Additionally, several innate immune subsets, which promote Th1 and Th17 responses and are implicated in the pathogenesis of IBD, have recently been identified in the human intestinal mucosa. The demonstration of both murine and human intestinal innate immune subsets contributing to regulation of adaptive immunity emphasizes the conserved innate immune functions across species and might promote development of the intestinal innate immunity-based clinical therapy.
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Regulation of Intestinal Homeostasis by Innate Immune Cells
Hisako Kayama,Junichi Nishimura,Kiyoshi Takeda 대한면역학회 2013 Immune Network Vol.13 No.6
The intestinal immune system has an ability to distinguish between the microbiota and pathogenic bacteria, and then activate pro-inflammatory pathways against pathogens for host defense while remaining unresponsive to the microbiota and dietary antigens. In the intestine, abnormal activation of innate immunity causes development of several inflammatory disorders such as inflammatory bowel diseases (IBD). Thus, activity of innate immunity is finely regulated in the intestine. To date, multiple innate immune cells have been shown to maintain gut homeostasis by preventing inadequate adaptive immune responses in the murine intestine. Additionally, several innate immune subsets, which promote Th1 and Th17 responses and are implicated in the pathogenesis of IBD, have recently been identified in the human intestinal mucosa. The demonstration of both murine and human intestinal innate immune subsets contributing to regulation of adaptive immunity emphasizes the conserved innate immune functions across species and might promote development of the intestinal innate immunity-based clinical therapy.
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Ohshima, Jun,Lee, Youngae,Sasai, Miwa,Saitoh, Tatsuya,Su Ma, Ji,Kamiyama, Naganori,Matsuura, Yoshiharu,Pann-Ghill, Suh,Hayashi, Mikako,Ebisu, Shigeyuki,Takeda, Kiyoshi,Akira, Shizuo,Yamamoto, Masahiro The American Association of Immunologists, Inc. 2014 JOURNAL OF IMMUNOLOGY Vol.192 No.7
<P>IFN-γ mediates cellular innate immunity against an intracellular parasite, <I>Toxoplasma gondii</I>, by inducing immunity-related GTPases such as p47 IFN-γ–regulated GTPases (IRGs) and p65 guanylate-binding proteins (GBPs), which also participate in antibacterial responses via autophagy. An essential autophagy protein, Atg5, was previously shown to play a critical role in anti–<I>T. gondii</I> cell-autonomous immunity. However, the involvement of other autophagy proteins remains unknown. In this study, we show that essential autophagy proteins differentially participate in anti–<I>T. gondii</I> cellular immunity by recruiting IFN-γ–inducible GTPases. IFN-γ–induced suppression of <I>T. gondii</I> proliferation and recruitment of an IRG Irgb6 and GBPs are profoundly impaired in Atg7- or Atg16L1-deficient cells. In contrast, cells lacking other essential autophagy proteins, Atg9a and Atg14, are capable of mediating the anti–<I>T. gondii</I> response and recruiting Irgb6 and GBPs to the parasites. Although IFN-γ also stimulates anti–<I>T. gondii</I> cellular immunity in humans, whether this response requires GBPs and human autophagy proteins remains to be seen. To analyze the role of human ATG16L1 and GBPs in IFN-γ–mediated anti–<I>T. gondii</I> responses, human cells lacking ATG16L1 or GBPs were generated by the Cas9/CRISPR genome-editing technique. Although both ATG16L1 and GBPs are dispensable for IFN-γ–induced inhibition of <I>T. gondii</I> proliferation in the human cells, human ATG16L1 is also required for the recruitment of GBPs. Taken together, human ATG16L1 and mouse autophagy components Atg7 and Atg16L1, but not Atg9a and Atg14, participate in the IFN-γ–induced recruitment of the immunity-related GTPases to the intracellular pathogen.</P>
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