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  • 1 Max Planck Institute for Infection Biology, Charitéplatz 1, 10117 Berlin, Germany
  • 2 Charité — Universitätsmedizin Berlin, Hindenburgdamm 30, 12200 Berlin, Germany
  • 3 Robert Koch-Institute, Berlin, Germany
  • 4 Charité — Universitätsmedizin Berlin, 12203 Berlin, Germany

Direct effects of Helicobacter pylori (H. pylori) on human CD4+ T-cells hamper disentangling a possible bacterial-mediated interference with major histocompatibility complex class II (MHC-II)-dependent antigen presentation to these cells. To overcome this limitation, we employed a previously described assay, which enables assessing human antigen-processing cell function by using murine T-cell hybridoma cells restricted by human leukocyte antigen (HLA) alleles. HLA-DR1+ monocyte-derived dendritic cells were exposed to H. pylori and pulsed with the antigen 85B from Mycobacterium tuberculosis (M. tuberculosis). Interleukin-2 (IL-2) secretion by AG85Baa97-112-specific hybridoma cells was then evaluated as an integral reporter of cognate antigen presentation. This methodology enabled revealing of interference of H. pylori with the antigen-presenting capacity of human dendritic cells.

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