T-bet in disease

Nat Immunol. 2011 Jun 20;12(7):597-606. doi: 10.1038/ni.2059.


The activation of immune-defense mechanisms in response to a microbial attack must be robust and appropriately tailored to fight particular types of pathogens. Infection with intracellular microorganisms elicits a type 1 inflammatory response characterized by mobilization of T helper type 1 (T(H)1) cells to the site of infection, where they are responsible for the recruitment and activation of macrophages. At the center of the type 1 inflammatory response is the transcription factor T-bet, a critical regulator of the T(H)1 differentiation program. T-bet induces the production of interferon-γ (IFN-γ) and orchestrates the T(H)1 cell-migratory program by regulating the expression of chemokines and chemokine receptors. However, tight regulation of the type 1 inflammatory response is essential for the prevention of immunopathology and the development of organ-specific autoimmunity. In this review, we discuss how T-bet expression drives autoaggressive and inflammatory processes and how its function in vivo must be delicately balanced to avoid disease.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Asthma / immunology
  • Autoimmune Diseases / immunology
  • Communicable Diseases / immunology*
  • Humans
  • Immunity, Cellular
  • Inflammation / immunology
  • Lymphocyte Activation / immunology
  • Macrophages / immunology
  • Mice
  • T-Box Domain Proteins / immunology*
  • T-Lymphocytes, Helper-Inducer / immunology


  • T-Box Domain Proteins
  • T-box transcription factor TBX21