Journal
CYTOKINE
Volume 77, Issue -, Pages 196-202Publisher
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.cyto.2015.09.005
Keywords
Q fever; Coxiella burnetii; Toll-like receptor 10; Single nucleotide polymorphism; Innate immunity
Funding
- Netherlands Organization for Health Research and Development [205520004, 205520002]
- European Research Council (ERC) [310372]
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Coxiella burnetii, the causative agent of Q fever, is recognized by TLR2. TLR10 can act as an inhibitory receptor on TLR2-derived immune responses. Therefore, we investigated the role of TLR10 on C. burnetii-induced cytokine production and assessed whether genetic polymorphisms in TLR10 influences the development of chronic Q fever. HEK293 cells, transfected with TLR2, TLR10 or TLR2/TLR10, and human peripheral blood mononuclear cells (PBMCs) in the presence of anti-TLR10, were stimulated with C burnetii. In both assays, the absence of TLR10 resulted in increased cytokine responses after C burnetii stimulation. In addition, the effect of single nucleotide polymorphisms (SNPs) in TLR10 was examined in healthy volunteers whose PBMCs were stimulated with C burnetii Nine Mile or the Dutch outbreak isolate C burnetii 3262. Individuals bearing SNPs in TLR10 displayed increased cytokine production upon C burnetii 3262 stimulation. Furthermore, 139 chronic Q fever patients and 220 controls were genotyped for TLR10 N241H, 1775V and I369L. None of these polymorphisms were associated with increased susceptibility to chronic Q fever. In conclusion, TLR10 has an inhibitory effect on in vitro cytokine production by C. burnetii, but the presence of TLR10 polymorphisms does not lead to an increased risk of developing chronic Q fever. (C) 2015 Elsevier Ltd. All rights reserved.
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