Bacterial infections promote T cell recognition of self-glycolipids.
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 Pam3CysSerLys4 (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.
De Libero
Gennaro
G
Experimental Immunology, Department of Research, University Hospital, Basel CH-4031, Switzerland. gennaro.delibero@unibas.ch
Moran
Anthony P
AP
Gober
Hans-Jürgen
HJ
Rossy
Emmanuel
E
Shamshiev
Abdijapar
A
Chelnokova
Olga
O
Mazorra
Zaima
Z
Vendetti
Silvia
S
Sacchi
Alessandra
A
Prendergast
Martina M
MM
Sansano
Sebastiano
S
Tonevitsky
Alexander
A
Landmann
Regine
R
Mori
Lucia
L
D000818:Animals; D017951:Antigen Presentation / Q000276:immunology; D000938:Antigen-Presenting Cells / Q000276:immunology; D018949:Antigens, CD1 / Q000276:immunology; D001324:Autoantigens / Q000276:immunology*; D015551:Autoimmunity; D001424:Bacterial Infections / Q000276:immunology*; D006017:Glycolipids / Q000276:immunology*; D006801:Humans; D008213:Lymphocyte Activation / Q000276:immunology; D013601:T-Lymphocytes / Q000276:immunology*
D018949:Antigens, CD1; D001324:Autoantigens; D006017:Glycolipids