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1 Department of Zoology, University of Oxford, Tinbergen Building, South Parks Road, Oxford OX1 3PS, UK. prasadabnave@gmail.com.
2 Department of Radiotherapy Oncology, CHU de la Timone, Assistance Publique-Hopitaux Marseille, 13385 Marseille, France. xavier.muracciole@gmail.com.
3 Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes (URMITE), Institut Hospitalier Universitaire Méditerranée-Infection, 19-21 Bd Jean Moulin, CEDEX 05, 13385 Marseille, France. eric.ghigo@gmail.com.
1 Department of Zoology, University of Oxford, Tinbergen Building, South Parks Road, Oxford OX1 3PS, UK. prasadabnave@gmail.com.
2 Department of Radiotherapy Oncology, CHU de la Timone, Assistance Publique-Hopitaux Marseille, 13385 Marseille, France. xavier.muracciole@gmail.com.
3 Unité de Recherche sur les Maladies Infectieuses et Tropicales Emergentes (URMITE), Institut Hospitalier Universitaire Méditerranée-Infection, 19-21 Bd Jean Moulin, CEDEX 05, 13385 Marseille, France. eric.ghigo@gmail.com.
A small gram-negative bacterium, Coxiella burnetii (C. burnetii), is responsible for a zoonosis called Q fever. C. burnetii is an intracellular bacterium that can survive inside microbicidal cells like monocytes and macrophages by hijacking several functions of the immune system. Among several virulence factors, the lipopolysaccharide (LPS) of C. burnetii is one of the major factors involved in this immune hijacking because of its atypical composition and structure. Thus, the aim of this mini-review is to summarize the repressive effects of C. burnetii LPS on the antibacterial immunity of cells.
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