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  1. AU="Toshiya Takahashi"
  2. AU=Hickey Chelsea L.
  3. AU="Badhrinarayanan, Shreya"
  4. AU="Milani, Liliana"
  5. AU="Reinhardt, Klaus"
  6. AU="Caudillo-Flores, Uriel"
  7. AU="Yin, Yizhen"
  8. AU=Kaushansky Kenneth
  9. AU="Golla, Jaya Prakash"
  10. AU="Penn, Marc S"
  11. AU="Montero, Vincent"
  12. AU="Etevenon, Pierre"
  13. AU="Hyseni, Agon"
  14. AU="Seitzman, Natalie"
  15. AU="Loukil, Abdelhalim"
  16. AU="Giammusso, Bruno"
  17. AU="Kaplan, Jonathan E"
  18. AU=Francolini Giulio
  19. AU="Yuhu Li"
  20. AU=Kim Moojung
  21. AU="Vise, Luciana M"
  22. AU="Marcinowska, Zuzanna"
  23. AU="Graff, Pablo"

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  1. Artikel ; Online: Psoriasis and Antimicrobial Peptides

    Toshiya Takahashi / Kenshi Yamasaki

    International Journal of Molecular Sciences, Vol 21, Iss 6791, p

    2020  Band 6791

    Abstract: Psoriasis is a systemic inflammatory disease caused by crosstalk between various cells such as T cells, neutrophils, dendritic cells, and keratinocytes. Antimicrobial peptides (AMPs) such as β-defensin, S100, and cathelicidin are secreted from these ... ...

    Abstract Psoriasis is a systemic inflammatory disease caused by crosstalk between various cells such as T cells, neutrophils, dendritic cells, and keratinocytes. Antimicrobial peptides (AMPs) such as β-defensin, S100, and cathelicidin are secreted from these cells and activate the innate immune system through various mechanisms to induce inflammation, thus participating in the pathogenesis of psoriasis. In particular, these antimicrobial peptides enhance the binding of damage-associated molecular patterns such as self-DNA and self-RNA to their receptors and promote the secretion of interferon from activated plasmacytoid dendritic cells and keratinocytes to promote inflammation in psoriasis. Neutrophil extracellular traps (NETs), complexes of self-DNA and proteins including LL-37 released from neutrophils in psoriatic skin, induce Th17. Activated myeloid dendritic cells secrete a mass of inflammatory cytokines such as IL-12 and IL-23 in psoriasis, which is indispensable for the proliferation and survival of T cells that produce IL-17. AMPs enhance the production of some of Th17 and Th1 cytokines and modulate receptors and cellular signaling in psoriasis. Inflammation induced by DAMPs, including self-DNA and RNA released due to microinjuries or scratches, and the enhanced recognition of DAMPs by AMPs, may be involved in the mechanism underlying the Köbner phenomenon in psoriasis.
    Schlagwörter psoriasis ; antimicrobial peptides ; β-defensin ; S100 proteins ; cathelicidin (LL-37) ; DAMPs ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2020-09-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: The Antimicrobial Peptide Cathelicidin Exerts Immunomodulatory Effects via Scavenger Receptors

    Ryo Amagai / Toshiya Takahashi / Hitoshi Terui / Taku Fujimura / Kenshi Yamasaki / Setsuya Aiba / Yoshihide Asano

    International Journal of Molecular Sciences, Vol 24, Iss 1, p

    2023  Band 875

    Abstract: An active form of cathelicidin antimicrobial peptide, LL-37, has immunomodulatory and stimulatory effects, though the specific pathways are not clear. The purpose of this study was to identify the cellular pathways by which LL-37 amplifies the ... ...

    Abstract An active form of cathelicidin antimicrobial peptide, LL-37, has immunomodulatory and stimulatory effects, though the specific pathways are not clear. The purpose of this study was to identify the cellular pathways by which LL-37 amplifies the inflammation induced by damage-associated molecular patterns (DAMPs). We performed DNA microarray, reverse transcription polymerase chain reaction, immunoblotting, and proximity ligation assays using cultured keratinocytes treated with LL-37 and/or the DAMP poly(I:C), a synthetic double-stranded RNA. In contrast to the combination of LL-37 and poly(I:C), LL-37 alone induced genes related to biological metabolic processes such as VEGFA and PTGS2 (COX-2). Inhibition of FPR2, a known receptor for cathelicidin, partially suppressed the induction of VEGFA and PTGS2. Importantly, VEGFA and PTGS2 induced by LL-37 alone were diminished by the knockdown of scavenger receptors including SCARB1 (SR-B1), OLR1 (SR-E1), and AGER (SR-J1). Moreover, LL-37 alone, as well as the combination of LL-37 and poly(I:C), showed proximity to the scavenger receptors, indicating that LL-37 acts via scavenger receptors and intermediates between them and poly(I:C). These results showed that the broad function of cathelicidin is generally dependent on scavenger receptors. Therefore, inhibitors of scavenger receptors or non-functional mock cathelicidin peptides may serve as new anti-inflammatory and immunosuppressive agents.
    Schlagwörter cathelicidin ; scavenger receptors ; damage-associated molecular patterns (DAMPs) ; psoriasis ; innate immunity ; Biology (General) ; QH301-705.5 ; Chemistry ; QD1-999
    Sprache Englisch
    Erscheinungsdatum 2023-01-01T00:00:00Z
    Verlag MDPI AG
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Cathelicidin promotes inflammation by enabling binding of self-RNA to cell surface scavenger receptors

    Toshiya Takahashi / Nikhil Nitin Kulkarni / Ernest Y Lee / Ling-juan Zhang / Gerard C. L. Wong / Richard L. Gallo

    Scientific Reports, Vol 8, Iss 1, Pp 1-

    2018  Band 13

    Abstract: Abstract Under homeostatic conditions the release of self-RNA from dying cells does not promote inflammation. However, following injury or inflammatory skin diseases such as psoriasis and rosacea, expression of the cathelicidin antimicrobial peptide LL37 ...

    Abstract Abstract Under homeostatic conditions the release of self-RNA from dying cells does not promote inflammation. However, following injury or inflammatory skin diseases such as psoriasis and rosacea, expression of the cathelicidin antimicrobial peptide LL37 breaks tolerance to self-nucleic acids and triggers inflammation. Here we report that LL37 enables keratinocytes and macrophages to recognize self-non-coding U1 RNA by facilitating binding to cell surface scavenger receptors that enable recognition by nucleic acid pattern recognition receptors within the cell. The interaction of LL37 with scavenger receptors was confirmed in human psoriatic skin, and the ability of LL37 to stimulate expression of interleukin-6 and interferon-β1 was dependent on a 3-way binding interaction with scavenger receptors and subsequent clathrin-mediated endocytosis. These results demonstrate that the inflammatory activity of LL37 is mediated by a cell-surface-dependent interaction and provides important new insight into mechanisms that drive auto-inflammatory responses in the skin.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2018-03-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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