de.mpg.escidoc.pubman.appbase.FacesBean
Deutsch
 
Hilfe Wegweiser Impressum Kontakt Einloggen
  DetailsucheBrowse

Datensatz

DATENSATZ AKTIONENEXPORT

Freigegeben

Zeitschriftenartikel

Autoregulation of Th1-mediated inflammation by twist1

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons50363

Janitz,  Michal
Dept. of Vertebrate Genomics (Head: Hans Lehrach), Max Planck Institute for Molecular Genetics, Max Planck Society;

Externe Ressourcen
Es sind keine Externen Ressourcen verfügbar
Volltexte (frei zugänglich)
Es sind keine frei zugänglichen Volltexte verfügbar
Ergänzendes Material (frei zugänglich)
Es sind keine frei zugänglichen Ergänzenden Materialien verfügbar
Zitation

Niesner, U., Albrecht, I., Janke, M., Doebis, C., Loddenkemper, C., Lexberg, M. H., et al. (2008). Autoregulation of Th1-mediated inflammation by twist1. Journal of Experimental Medicine, 205(8), 1889-1901. doi:10.1084/jem.20072468.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-7F5D-6
Zusammenfassung
The basic helix-loop-helix transcriptional repressor twist1, as an antagonist of nuclear factor {kappa}B (NF-{kappa}B)–dependent cytokine expression, is involved in the regulation of inflammation-induced immunopathology. We show that twist1 is expressed by activated T helper (Th) 1 effector memory (EM) cells. Induction of twist1 in Th cells depended on NF-{kappa}B, nuclear factor of activated T cells (NFAT), and interleukin (IL)-12 signaling via signal transducer and activator of transcription (STAT) 4. Expression of twist1 was transient after T cell receptor engagement, and increased upon repeated stimulation of Th1 cells. Imprinting for enhanced twist1 expression was characteristic of repeatedly restimulated EM Th cells, and thus of the pathogenic memory Th cells characteristic of chronic inflammation. Th lymphocytes from the inflamed joint or gut tissue of patients with rheumatic diseases, Crohn's disease or ulcerative colitis expressed high levels of twist1. Expression of twist1 in Th1 lymphocytes limited the expression of the cytokines interferon-{gamma}, IL-2, and tumor necrosis factor-{alpha}, and ameliorated Th1-mediated immunopathology in delayed-type hypersensitivity and antigen-induced arthritis.