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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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De Libero, G. et al.

De Libero, Moran, Gober, Rossy, Shamshiev, Chelnokova, Mazorra, Vendetti, Sacchi, Prendergast, Sansano, Tonevitsky, Landmann, Mori,

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 GuerÃn [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.[1]

References

Bacterial infections promote T cell recognition of self-glycolipids. De Libero, G., Moran, A.P., Gober, H.J., Rossy, E., Shamshiev, A., Chelnokova, O., Mazorra, Z., Vendetti, S., Sacchi, A., Prendergast, M.M., Sansano, S., Tonevitsky, A., Landmann, R., Mori, L. Immunity (2005) [Pubmed]

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