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. Copyright ©2005 by Elsevier Inc.
De Libero, G., Moran, A.P., Gober, H.-., Rossy, E., Shamshiev, A., Chelnokova, O., et al. (2005). Bacterial infections promote T cell recognition of self-glycolipids. IMMUNITY, 22(6), 763-772 [10.1016/j.immuni.2005.04.013].
Bacterial infections promote T cell recognition of self-glycolipids
Sacchi A.;
2005-01-01
Abstract
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. Copyright ©2005 by Elsevier Inc.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
