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  1. AU="Levasseur, Franck"
  2. AU="Arianna Rubin Means"
  3. AU="Murdan, Sudaxshina"
  4. AU=Kimberley Fiona C
  5. AU="Solís, José Gabriel"
  6. AU="Becker, Maximilian R"
  7. AU="Alasonati, Enrica"
  8. AU="Arribas, Silvia Magdalena"
  9. AU=Edry Efrat
  10. AU="James B. McCauley"
  11. AU="Offringa, Ite A"
  12. AU="Sakso, Salima Ahriz"
  13. AU="Huang, Zexiang"
  14. AU="Feleke, Sindew M"
  15. AU="van der Velden, Janielle"
  16. AU="Carmen Gonzalez"
  17. AU="Cheah, Jaime H"
  18. AU="Forte, Florence"
  19. AU="Anika Nier"
  20. AU="Bar, Adi"
  21. AU="Alvarado Pinedo, María F."
  22. AU="Scarlett, Garry"
  23. AU="Carlos G. Vanoye"
  24. AU=Lohrmann Jens
  25. AU="Petersen, Moritz"
  26. AU="Giovanni, L."
  27. AU="Liu, Xingzheng"
  28. AU="Głód, Mateusz"
  29. AU=Teo Kelvin Yi Chong
  30. AU="Khatmi, Aysan"
  31. AU="Erculiani, M"
  32. AU="Olivier Lortholary"
  33. AU="Lisnic, Vanda Juranic"
  34. AU="Seabloom, Eric W"
  35. AU="Odvina, Clarita V"
  36. AU="Singh, Inderbir"
  37. AU="Wonoh Lee"
  38. AU="Nelson, Warrick"
  39. AU="Douglas, David N"
  40. AU="King, Gary"
  41. AU="Barbera, Lauren"
  42. AU="Carlino, Antonio"
  43. AU="Shan, Qing-Hua"
  44. AU="Starko, S"
  45. AU="Lievre, Loïc"
  46. AU=Cammack N
  47. AU="Xia, Qin"
  48. AU="Ong, Ju Lynn"
  49. AU="Cullin, Christophe"
  50. AU="Georg K.S. Andersson"
  51. AU="Jeannel, Gaël-François"
  52. AU="Stuart Woods"
  53. AU="Shchegolev, A."
  54. AU="Nadeau, Pierre-Louis"
  55. AU="Gordon, David E A"
  56. AU="Shahid Mahmood"
  57. AU="Rosenblatt, Karin"
  58. AU="Dasgupta, Suvankar"
  59. AU=Nguyen Sylvain AU=Nguyen Sylvain

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  1. Artikel ; Online: Antibody-mediated neutralization of galectin-3 as a strategy for the treatment of systemic sclerosis.

    Ortega-Ferreira, Céline / Soret, Perrine / Robin, Gautier / Speca, Silvia / Hubert, Sandra / Le Gall, Marianne / Desvaux, Emiko / Jendoubi, Manel / Saint-Paul, Julie / Chadli, Loubna / Chomel, Agnès / Berger, Sylvie / Nony, Emmanuel / Neau, Béatrice / Fould, Benjamin / Licznar, Anne / Levasseur, Franck / Guerrier, Thomas / Elouej, Sahar /
    Courtade-Gaïani, Sophie / Provost, Nicolas / Nguyen, The Quyen / Verdier, Julien / Launay, David / De Ceuninck, Frédéric

    Nature communications

    2023  Band 14, Heft 1, Seite(n) 5291

    Abstract: Systemic sclerosis (SSc) is an autoimmune, inflammatory and fibrotic disease with limited treatment options. Developing new therapies is therefore crucial to address patient needs. To this end, we focused on galectin-3 (Gal-3), a lectin known to be ... ...

    Abstract Systemic sclerosis (SSc) is an autoimmune, inflammatory and fibrotic disease with limited treatment options. Developing new therapies is therefore crucial to address patient needs. To this end, we focused on galectin-3 (Gal-3), a lectin known to be associated with several pathological processes seen in SSc. Using RNA sequencing of whole-blood samples in a cross-sectional cohort of 249 patients with SSc, Gal-3 and its interactants defined a strong transcriptomic fingerprint associated with disease severity, pulmonary and cardiac malfunctions, neutrophilia and lymphopenia. We developed new Gal-3 neutralizing monoclonal antibodies (mAb), which were then evaluated in a mouse model of hypochlorous acid (HOCl)-induced SSc. We show that two of these antibodies, D11 and E07, reduced pathological skin thickening, lung and skin collagen deposition, pulmonary macrophage content, and plasma interleukin-5 and -6 levels. Moreover, E07 changed the transcriptional profiles of HOCl-treated mice, resulting in a gene expression pattern that resembled that of control mice. Similarly, pathological pathways engaged in patients with SSc were counteracted by E07 in mice. Collectively, these findings demonstrate the translational potential of Gal-3 blockade as a therapeutic option for SSc.
    Mesh-Begriff(e) Animals ; Mice ; Galectin 3/genetics ; Cross-Sectional Studies ; Scleroderma, Systemic/drug therapy ; Scleroderma, Systemic/genetics ; Antibodies, Monoclonal ; Disease Models, Animal ; Hypochlorous Acid
    Chemische Substanzen Galectin 3 ; Antibodies, Monoclonal ; Hypochlorous Acid (712K4CDC10)
    Sprache Englisch
    Erscheinungsdatum 2023-08-31
    Erscheinungsland England
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-023-41117-9
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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  2. Artikel ; Online: Hepatitis C virus (HCV) evades NKG2D-dependent NK cell responses through NS5A-mediated imbalance of inflammatory cytokines.

    Sène, Damien / Levasseur, Franck / Abel, Michal / Lambert, Marion / Camous, Xavier / Hernandez, Céline / Pène, Véronique / Rosenberg, Arielle R / Jouvin-Marche, Evelyne / Marche, Patrice N / Cacoub, Patrice / Caillat-Zucman, Sophie

    PLoS pathogens

    2010  Band 6, Heft 11, Seite(n) e1001184

    Abstract: Understanding how hepatitis C virus (HCV) induces and circumvents the host's natural killer (NK) cell-mediated immunity is of critical importance in efforts to design effective therapeutics. We report here the decreased expression of the NKG2D activating ...

    Abstract Understanding how hepatitis C virus (HCV) induces and circumvents the host's natural killer (NK) cell-mediated immunity is of critical importance in efforts to design effective therapeutics. We report here the decreased expression of the NKG2D activating receptor as a novel strategy adopted by HCV to evade NK-cell mediated responses. We show that chronic HCV infection is associated with expression of ligands for NKG2D, the MHC class I-related Chain (MIC) molecules, on hepatocytes. However, NKG2D expression is downmodulated on circulating NK cells, and consequently NK cell-mediated cytotoxic capacity and interferon-γ production are impaired. Using an endotoxin-free recombinant NS5A protein, we show that NS5A stimulation of monocytes through Toll-like Receptor 4 (TLR4) promotes p38- and PI3 kinase-dependent IL-10 production, while inhibiting IL-12 production. In turn, IL-10 triggers secretion of TGFβ which downmodulates NKG2D expression on NK cells, leading to their impaired effector functions. Moreover, culture supernatants of HCV JFH1 replicating Huh-7.5.1 cells reproduce the effect of recombinant NS5A on NKG2D downmodulation. Exogenous IL-15 can antagonize the TGFβ effect and restore normal NKG2D expression on NK cells. We conclude that NKG2D-dependent NK cell functions are modulated during chronic HCV infection, and demonstrate that this alteration can be prevented by exogenous IL-15, which could represent a meaningful adjuvant for therapeutic intervention.
    Mesh-Begriff(e) Adult ; Aged ; Cytokines/metabolism ; Cytotoxicity, Immunologic ; Female ; Flow Cytometry ; Hepacivirus/immunology ; Hepatitis C, Chronic/immunology ; Hepatitis C, Chronic/metabolism ; Humans ; Immunity, Cellular ; Inflammation Mediators/metabolism ; Killer Cells, Natural/immunology ; Killer Cells, Natural/metabolism ; Liver Cirrhosis/immunology ; Liver Cirrhosis/metabolism ; Liver Cirrhosis/pathology ; Male ; Middle Aged ; Monocytes/cytology ; Monocytes/metabolism ; NK Cell Lectin-Like Receptor Subfamily K/metabolism ; Viral Nonstructural Proteins/metabolism ; Virus Replication ; Young Adult
    Chemische Substanzen Cytokines ; Inflammation Mediators ; NK Cell Lectin-Like Receptor Subfamily K ; Viral Nonstructural Proteins ; NS-5 protein, hepatitis C virus (EC 2.7.7.48)
    Sprache Englisch
    Erscheinungsdatum 2010-11-11
    Erscheinungsland United States
    Dokumenttyp Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2205412-1
    ISSN 1553-7374 ; 1553-7366
    ISSN (online) 1553-7374
    ISSN 1553-7366
    DOI 10.1371/journal.ppat.1001184
    Datenquelle MEDical Literature Analysis and Retrieval System OnLINE

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    Dieser Service ist kostenpflichtig (siehe Lieferbedingungen von subito). Bestellungen, die einen Artikel nebst Supplementary Material umfassen, werden grundsätzlich wie mehrfache Bestellungen bearbeitet. Gebühren fallen in diesen Fällen für jede einzelne Bestellung an.

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