Bacterial infections promote T cell recognition of self-glycolipids

Gennaro De Libero, Anthony P. Moran, Hans Jürgen Gober, Emmanuel Rossy, Abdijapar Shamshiev, Olga Chelnokova, Zaima Mazorra, Silvia Vendetti, Alessandra Sacchi, Martina M. Prendergast, Sebastiano Sansano, Alexander Tonevitsky, Regine Landmann, Lucia Mori

Research output: Contribution to journalArticlepeer-review


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.

Original languageEnglish
Pages (from-to)763-772
Number of pages10
Issue number6
Publication statusPublished - Jun 2005

ASJC Scopus subject areas

  • Immunology and Allergy
  • Infectious Diseases
  • Immunology


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