select ad.sno,ad.journal,ad.title,ad.author_names,ad.abstract,ad.abstractlink,j.j_name,vi.* from articles_data ad left join journals j on j.journal=ad.journal left join vol_issues vi on vi.issue_id_en=ad.issue_id where ad.sno_en='48484' and ad.lang_id='5' and j.lang_id='5' and vi.lang_id='5' New Paradigm of T cell Signaling: Learning from Malignancies | 48484
Journal d'immunologie clinique et cellulaire

Journal d'immunologie clinique et cellulaire
Libre accès

ISSN: 2155-9899

Abstrait

New Paradigm of T cell Signaling: Learning from Malignancies

Makoto Yamagishi and Toshiki Watanabe

T cells are key mediators of cell-mediated immunity. Their functions and proliferation result from T cell-specific receptor signaling (TCR/CD28) that activates the NF-κB, NFAT, Ras-MAPK, and PI3K-Akt pathways. Their development and activation also involve a complex array of signaling pathways that regulate gene expression networks, including signaling of mTOR, Notch, Wnt, Hedgehog, TGF-β, and toll-like receptors. Furthermore, recent discoveries have provided two molecular hallmarks of potential generality: miRNA patterns and polycomb-mediated epigenetic reprogramming, which can strongly coordinate the balance between molecular networks in lymphocytes. Their deregulation apparently causes T cell disorders, such as T cell acute lymphoblastic leukemia (T-ALL), and human T cell leukemia virus (HTLV-1)-induced adult T cell leukemia (ATL). This review continues with a description of our understanding of crosstalk among the signaling pathways, which contribute to the highly orchestrated development of T cell fate specification under both normal physiological and pathological conditions.

Clause de non-responsabilité: Ce résumé a été traduit à l'aide d'outils d'intelligence artificielle et n'a pas encore été révisé ou vérifié.
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