Taniki, Nobuhito

写真a

Affiliation

School of Medicine, Department of Internal Medicine (Gastroenterology and Hepatology) (Shinanomachi)

Position

Senior Assistant Professor (Non-tenured)/Assistant Professor (Non-tenured)
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  • Enrichment of type I interferon signaling in colonic group 2 innate lymphoid cells in experimental colitis

    Irie E., Ishihara R., Mizushima I., Hatai S., Hagihara Y., Takada Y., Tsunoda J., Iwata K., Matsubara Y., Yoshimatsu Y., Kiyohara H., Taniki N., Sujino T., Takabayashi K., Hosoe N., Ogata H., Teratani T., Nakamoto N., Mikami Y., Kanai T.

    Frontiers in Immunology (Frontiers in Immunology)  13   982827 2022.10

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    Group 2 innate lymphoid cells (ILC2s) serve as frontline defenses against parasites. However, excluding helminth infections, it is poorly understood how ILC2s function in intestinal inflammation, including inflammatory bowel disease. Here, we analyzed the global gene expression of ILC2s in healthy and colitic conditions and revealed that type I interferon (T1IFN)-stimulated genes were up-regulated in ILC2s in dextran sodium sulfate (DSS)-induced colitis. The enhancement of T1IFN signaling in ILC2s in DSS-induced colitis was correlated with the downregulation of cytokine production by ILC2s, such as interleukin-5. Blocking T1IFN signaling during colitis resulted in exaggeration of colitis in both wild-type and Rag2-deficient mice. The exacerbation of colitis induced by neutralization of T1IFN signaling was accompanied by reduction of amphiregulin (AREG) in ILC2s and was partially rescued by exogenous AREG treatment. Collectively, these findings show the potential roles of T1IFN in ILC2s that contribute to colitis manifestation.

  • Dynamics of type IV collagen 7S fragment on eradication of HCV with direct antiviral agents: Prognostic and metabolomic impacts

    Yamataka K., Chu P.S., Koda Y., Taniki N., Morikawa R., Yoshida A., Noguchi F., Kasuga R., Tabuchi T., Ebinuma H., Kanai T., Nakamoto N.

    PLoS ONE (PLoS ONE)  17 ( 10 October ) e0276925 2022.10

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    Background Liver fibrosis is one of the cardinal clinical features of chronic hepatitis C (CHC). However, the mechanisms underlying the evolution and reversion of liver fibrosis after hepatitis C virus (HCV) eradication and their relationship with clinical outcomes and metabolic alterations are not fully elucidated. Whether any non-invasive fibrosis marker can predict prognosis is unknown. Methods Between October 2014 and September 2019, 418 patients with CHC or compensated cirrhosis with HCV were prospectively recruited in this observational study. 326 patients that were successfully eradicated with interferon-free direct antiviral agents (IFN-free DAAs) were analyzed. Peri-treatment dynamics of serum levels of type IV collagen 7S fragment (4COL7S), a fibrosis marker, and subsequent clinical outcomes, including hepatic decompensation, newly emerged hepatocellular carcinoma (HCC), and all-cause mortality were analyzed. Results Ten (3.1%) patients died during the observation period. 4COL7S-defined fibrosis progression (n = 97, 29.8%) at SVR was significantly correlated with worse all-cause mortality post-SVR (P = 0.0062) but not with the probability of newly emerged HCC (P = 0.24). Prognostic tendency was more prominent in patients with advanced fibrosis (P< 0.0001). 4COL7S-defined fibrosis progression at SVR and a baseline platelet count less than 10×104/μL were significantly predicted all-cause mortality (P = 0.0051). In exploratory analyses, a decreased 4COL7S at the end of treatment was correlated with a matrix-degrading phenotype that showed higher serum metalloproteinase to tissue inhibitors of metalloproteinase-1 ratios and characteristic metabolic fingerprints such as increased butyrate, some medium-chain fatty acids, anabolic amino acids, and decreased uremia toxins. Conclusions Peri-treatment dynamics of serum 4COL7S, a non-invasive fibrosis marker, predict prognosis. Non-invasive fibrosis markers may be useful biomarkers for risk stratification post-SVR.

  • CCR9 axis inhibition enhances hepatic migration of plasmacytoid DCs and protects against liver injury

    Koda Y., Nakamoto N., Chu P.S., Teratani T., Ueno A., Amiya T., Taniki N., Chiba S., Miyamoto K., Sakamoto M., Kanai T.

    JCI Insight (JCI Insight)  7 ( 17 )  2022.09

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    Plasmacytoid dendritic cells (pDCs) perform dual proinflammatory and immunosuppressive roles. We recently reported the potential of pDC therapy for treatment of intractable acute liver failure. However, establishment of efficient methods to deliver pDCs to the liver is essential for future clinical therapeutic applications. The present study demonstrates a higher abundance of liver and peripheral blood pDCs in mice lacking C-C motif chemokine receptor 9 (CCR9), a pDC gut-homing receptor, than in WT mice. Adoptive transfer of Ccr9–/– pDCs resulted in a higher efficiency of migration to the liver than WT pDCs did, while WT pDCs migrated efficiently to the original target organ, the small intestine. Further, Ccr9–/– pDCs consistently migrated efficiently to livers with concanavalin A–induced inflammation, and exerted a more effective immunosuppressive effect, resulting in better protection against acute liver inflammation than that demonstrated by WT pDCs. These findings highlight the therapeutic potential of the manipulation of the CCR9 axis as an approach to improve migration of immunosuppressive pDCs to the liver in order to exploit their beneficial effects in acute liver disease.

  • Th17 cells in the liver: balancing autoimmunity and pathogen defense

    Taniki N., Nakamoto N., Chu P.S., Ichikawa M., Teratani T., Kanai T.

    Seminars in Immunopathology (Seminars in Immunopathology)  44 ( 4 ) 509 - 526 2022.07

    ISSN  18632297

    　View Summary

    In addition to carcinogenesis, T helper 17 (Th17) cells (a subtype of CD4 + T lymphocytes) are involved in the acute, chronic, and cirrhotic phases of liver diseases; however, their role in the development and progression of liver diseases remains unclear. It is difficult to elucidate the role of Th17 cells in liver diseases due to their dichotomous nature, i.e., plasticity in terms of pathogenic or host protective function depending on environmental and time phase factors. Moreover, insufficient depletion of Th17 cells by inhibiting the cytokines and transcription factors involved in their production causes difficulties in analyzing their specific role in vitro and in vivo murine models, partially due to complex interaction. This review summarizes the recent progress in understanding the plasticity and function of hepatic Th17 cells and type 3 cytokines.

  • Concurrent de novo Thymoma-associated Paraneoplastic Type 1 Autoimmune Hepatitis and Pure Red Cell Aplasia After Thymectomy: A Case Report and Literature Review.

    Sakata R, Chu PS, Kawaida M, Emoto K, Sakurai M, Nishida R, Asakura K, Morikawa R, Taniki N, Kataoka K, Kanai T, Nakamoto N

    Internal medicine (Tokyo, Japan)  2022.06

    ISSN  0918-2918

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Papers, etc., Registered in KOARA 【 Display / hide 】

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

  • "腸-肝臓-脳相関"で構成される自律神経回路による大腸癌の新規病態解明と治療開発

    2022.04
    -
    2025.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 基盤研究(C), Principal investigator

  • インジゴ化合物による新規原発性硬化性胆管炎治療法の開発

    2020.04
    -
    2022.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Early-Career Scientists , Principal investigator

  • 腸肝相関を介した肝免疫寛容誘導機序の解明

    2018.04
    -
    2020.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Early-Career Scientists , Principal investigator

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Courses Taught 【 Display / hide 】

  • PATHOPHYSIOLOGICAL ISSUES IN CHRONIC CARE

    2024

  • LECTURE SERIES, INTERNAL MEDICINE (GASTROENTEROLOGY)

    2024

  • PATHOPHYSIOLOGICAL ISSUES IN CHRONIC CARE

    2023

  • LECTURE SERIES, INTERNAL MEDICINE (GASTROENTEROLOGY)

    2023

  • LECTURE SERIES, INTERNAL MEDICINE (GASTROENTEROLOGY)

    2022

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