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Mycobacteria Induce IFN- Production in Human Dendritic Cells via Triggering of TLR2¹

Ingo Fricke^2,3,*, Daniell Mitchell^2,*, Jessica Mittelstädt^*, Nadine Lehan^*, Holger Heine, Torsten Goldmann, Andreas Böhle and Sven Brandau^4,*

^* Division of Immunotherapy, Division of Innate Immunity, and Division of Pathology, Research Center Borstel, Borstel, Germany; and Helios Agnes Karll Hospital, Bad Schwartau, Germany

IFN- is of central importance for the induction of robust cell-mediated immunity and for the activation of APC. Recent studies using experimental murine systems have now suggested a fundamental role for APC-derived IFN- during infection with intracellular pathogens. It is currently unknown whether human dendritic cells (DC) can respond to bacterial stimulation with production of IFN-. To test this question, we used human monocyte-derived DC stimulated by Mycobacterium bovis bacillus Calmette-Guérin as a model system. We demonstrate production of IFN- mRNA and protein on the single cell level. IFN- in DC cultures was not simply produced by contaminating lymphocytes because production of DC-IFN- could also be demonstrated in highly purified DC cultures containing virtually no T, B, and NK cells. TLR2 was identified as a key receptor involved in triggering production of DC-IFN-. Interestingly, DC-IFN- seems to participate in an autocrine DC activation loop, and production of DC-IFN- could be enhanced by costimulation of DC with IL-12/IL-15/IL-18. In conclusion, we have demonstrated production of IFN- by human DC on the single cell level, identified TLR2 as a pattern recognition receptor involved in this process, and elucidated some of the functional consequences of autocrine IFN- production by human DC.

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