T-cell effector pathways in allergic diseases: Transcriptional mechanisms and therapeutic targets

  • Chatila T
  • Li N
  • Garcia-Lloret M
 et al. 
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Abstract

Originally interpreted within the framework of a binary TH1/TH2 paradigm, our knowledge of the pathogenesis of atopic diseases has broadened to incorporate the contribution of T regulatory cells and the newly described proinflammatory TH17 cell lineage. The commitment of peripheral T-cell clones to undergo differentiation into one of those lineages is shaped by self-reinforcing transcriptional circuitries that center on key transcriptional regulators: T-box expressed in T cells (TH1), GATA-3 (TH2), forkhead box p3 (T regulatory cells), and retinoid-related orphan receptor γτ/retinoid-related orphan receptor α (TH17). These circuits function both to establish the respective lineage phenotype and to enable epigenetic changes that maintain those phenotypes long-term. This evolving view of how signaling and transcriptional networks generate effector T-cell responses suggests novel therapeutic approaches to reprogram effector T-cell lineage commitment in allergic diseases in favor of tolerance induction. © 2008 American Academy of Allergy, Asthma & Immunology.

Author-supplied keywords

  • Foxp3
  • GATA-3
  • Nrf2
  • RORγτ
  • T-bet
  • T-cell differentiation
  • TH1
  • TH17
  • TH2
  • Transcriptional regulation
  • Treg
  • asthma
  • atopic disease
  • oxidative stress
  • therapeutic strategies

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