T-bet is required for optimal proinflammatory CD4+ T-cell trafficking

Blood. 2005 Nov 15;106(10):3432-9. doi: 10.1182/blood-2005-04-1393. Epub 2005 Jul 12.

Abstract

Inflammatory responses are controlled by T helper 1 (Th1) lymphocytes. An important function of this polarity is the ability of T cells to traffick appropriately in vivo. This differential trafficking is dependent upon the binding of P-selectin glycoprotein ligand-1 to P- and E-selectin on inflamed endothelium as well as the expression of specific chemokine receptors. Here we show that in the absence of T-box expressed in T cells (T-bet), selective migration of T cells in vivo is completely abrogated and that T-bet regulates the binding of CD4(+) T cells to P-selectin. T-bet is also required for the expression of the chemokine receptor CXCR3. Thus, T-bet controls Th1-cell migration to inflammatory sites, which has fundamental consequences for the control of immunologic disease.

Publication types

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

MeSH terms

  • Animals
  • Cell Movement / genetics
  • Cell Movement / immunology*
  • Cells, Cultured
  • E-Selectin / immunology
  • E-Selectin / metabolism
  • Gene Expression Regulation / genetics
  • Gene Expression Regulation / immunology
  • Inflammation / genetics
  • Inflammation / immunology
  • Membrane Glycoproteins / immunology
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Inbred BALB C
  • Mice, Knockout
  • P-Selectin / immunology
  • P-Selectin / metabolism
  • Protein Binding / immunology
  • Receptors, Chemokine / genetics
  • Receptors, Chemokine / immunology
  • T-Box Domain Proteins
  • Th1 Cells / immunology*
  • Transcription Factors / genetics
  • Transcription Factors / immunology*
  • Transcription Factors / metabolism

Substances

  • E-Selectin
  • Membrane Glycoproteins
  • P-Selectin
  • P-selectin ligand protein
  • Receptors, Chemokine
  • T-Box Domain Proteins
  • T-box transcription factor TBX21
  • Transcription Factors