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 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.
journal_name
Immunityjournal_title
Immunityauthors
De Libero G,Moran AP,Gober HJ,Rossy E,Shamshiev A,Chelnokova O,Mazorra Z,Vendetti S,Sacchi A,Prendergast MM,Sansano S,Tonevitsky A,Landmann R,Mori Ldoi
10.1016/j.immuni.2005.04.013keywords:
subject
Has Abstractpub_date
2005-06-01 00:00:00pages
763-72issue
6eissn
1074-7613issn
1097-4180pii
S1074-7613(05)00165-2journal_volume
22pub_type
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