TY - JOUR
T1 - Bacterial infections promote T cell recognition of self-glycolipids
AU - De Libero, Gennaro
AU - Moran, Anthony P.
AU - Gober, Hans Jürgen
AU - Rossy, Emmanuel
AU - Shamshiev, Abdijapar
AU - Chelnokova, Olga
AU - Mazorra, Zaima
AU - Vendetti, Silvia
AU - Sacchi, Alessandra
AU - Prendergast, Martina M.
AU - Sansano, Sebastiano
AU - Tonevitsky, Alexander
AU - Landmann, Regine
AU - Mori, Lucia
PY - 2005/6
Y1 - 2005/6
N2 - Recognition of self is essential for repertoire selection, immune regulation, and autoimmunity and may be a consequence of infection. Self-induced recognition may represent the escape mechanism adopted by pathogens but may also incite autoimmune diseases. Here, we show that bacterial infection may promote activation of T cells reactive to self-glycosphingolipids (self-GSL). CD1+ antigen-presenting cells (APCs) infected with bacteria (Escherichia coli, Bacillus subtilis, Staphylococcus aureus, or Mycobacterium bovis-Bacillus Calmette Guerín [BCG]) or treated with the bacterial components lipopolysaccharide, lipoteichoic acid, or Pam 3CysSerLys4 (P3CSK4) lipopeptide acquire the capacity to stimulate self-GSL-specific T cells to cytokine release. Immediately after infection, APCs increase the endogenous GSL synthesis and stimulate GSL-specific T cells in a CD1- and T cell receptor (TCR)-dependent manner. This stimulation may contribute to inflammatory responses during bacterial infections and may predispose individuals to autoimmune diseases.
AB - Recognition of self is essential for repertoire selection, immune regulation, and autoimmunity and may be a consequence of infection. Self-induced recognition may represent the escape mechanism adopted by pathogens but may also incite autoimmune diseases. Here, we show that bacterial infection may promote activation of T cells reactive to self-glycosphingolipids (self-GSL). CD1+ antigen-presenting cells (APCs) infected with bacteria (Escherichia coli, Bacillus subtilis, Staphylococcus aureus, or Mycobacterium bovis-Bacillus Calmette Guerín [BCG]) or treated with the bacterial components lipopolysaccharide, lipoteichoic acid, or Pam 3CysSerLys4 (P3CSK4) lipopeptide acquire the capacity to stimulate self-GSL-specific T cells to cytokine release. Immediately after infection, APCs increase the endogenous GSL synthesis and stimulate GSL-specific T cells in a CD1- and T cell receptor (TCR)-dependent manner. This stimulation may contribute to inflammatory responses during bacterial infections and may predispose individuals to autoimmune diseases.
UR - https://www.scopus.com/pages/publications/20444440723
U2 - 10.1016/j.immuni.2005.04.013
DO - 10.1016/j.immuni.2005.04.013
M3 - Article
SN - 1074-7613
VL - 22
SP - 763
EP - 772
JO - Immunity
JF - Immunity
IS - 6
ER -
