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Male wild-type (m PPARα ), Pparα-null (Lee et al. 1995), and h PPARαTet-OFF (h PPARα) (Cheung et al. 2004) mice on an Sv/129 genetic background were bred as described elsewhere (Nakamura et al. 2009) and reared at the Institute of Laboratory Animal Research Nagoya University Graduate School of Medicinee).
TNFR1−/− NF-κB p65+/− mice and TNFR1−/− NF-κB p65+/+ on Bl6/129 background were bred as previous described (Quinton et al, 2007).
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All mice with 129/Sv genetic background were bred at l'institut du thorax (Nantes, France) and genotyped by polymerase chain reaction (PCR) as previously described [9].
Mice homozygously deficient in P2Y12 receptors [24] and corresponding wild types (C57BL/6 background) were bred and housed, as described previously [25].
Homozygous knockout (hereafter referred to as IL-23KO) and wild-type animals on the 129×C57BL/6 mixed background were bred and used in experiments.
ApoE−/− mice, also on a C57BL/6 background, were bred in house.
Mice on the C57Bl/6J background were bred in specific pathogen free conditions.
Crem−/−mice were bred as previously described [48].
Animals were bred as described earlier [ 15].
WT and heterozygous Thra1 PV /+ mice have a mixed C57BL/6J and NIH Black Swiss genetic background and were bred and genotyped as described elsewhere (14, 21).
Heterozygous transgenic mice crossed in C57Bl/6 background and expressing human CD150 [24] and their littermate controls, as well as CD150 transgenic mice crossed into Foxp3-GFP background [29] or in IFN Receptor α/β deficient background [43] were bred at the institute's animal facility (PBES) and infected at the age of 1 week.
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