Bacterial infections promote t cell recognition of self-glycolipids
De Libero, Gennaro
Moran, Anthony P.
Prendergast, Martina M.
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De Libero, Gennaro; Moran, Anthony P. Gober, Hans-Jürgen; Rossy, Emmanuel; Shamshiev, Abdijapar; Chelnokova, Olga; Mazorra, Zaima; Vendetti, Silvia; Sacchi, Alessandra; Prendergast, Martina M.; Sansano, Sebastiano; Tonevitsky, Alexander; Landmann, Regine; Mori, Lucia (2005). Bacterial infections promote t cell recognition of self-glycolipids. Immunity 22 (6), 763-772
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 Guerin [BCG]) or treated with the bacterial components lipopolysaccharide, lipoteichoic acid, or Pam(3)CysSerLys(4) (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.