Figure 4.
NAPc2 prevents the development of aPL in mCMV infection. (A) Blood cytokine levels of WT animals infected with 2 × 105 plaque-forming unit mCMV and treated with 0.5 mg/kg NAPc2 (red) or saline (blue) every second day. In contrast to the depicted significantly reduced cytokine levels 42 hours after infection, NAPc2 treatment had no effect on TNF, IL6, IL1β, IL10, and CCL5 expression measured in the same multiplex assay; ∗P< .05, ∗∗P< .01, 2-way ANOVA, Sidak comparison. (B) Viral loads determined by quantification of genomic viral DNA in the indicated organs 21 days after infection in mice treated from day 2 after viral infection. (C) Serum anti-CL titers were determined at the indicated times; n = 8 mice, ∗P ≤ .001; 2-way ANOVA, Sidak multiple comparisons test. (D) Fluorescent PL vesicles staining of circulating B cells at day 10 after infection. PL-positive B cells were identified as CD5+CD19+CD27+CD43+ memory type B1a cells in peripheral blood and absent in NAPc2-treated mice. (E) Quantification of blood PL+ CD19+ B cells in mice treated with NAPc2 or saline control at day 10. Mean ± SD, n = 8 mice, ∗P < .0001, t test following Shapiro-Wilk test for normal distribution (F) serum anti-LBPA and anti-β2GPI titers were determined 12 weeks after infection and NAPc2 treatment for 20 days. n = 6 to 7 mice, ∗P ≤ .0001; 2-way ANOVA, Sidak multiple comparisons test.

NAPc2 prevents the development of aPL in mCMV infection. (A) Blood cytokine levels of WT animals infected with 2 × 105 plaque-forming unit mCMV and treated with 0.5 mg/kg NAPc2 (red) or saline (blue) every second day. In contrast to the depicted significantly reduced cytokine levels 42 hours after infection, NAPc2 treatment had no effect on TNF, IL6, IL1β, IL10, and CCL5 expression measured in the same multiplex assay; ∗P< .05, ∗∗P< .01, 2-way ANOVA, Sidak comparison. (B) Viral loads determined by quantification of genomic viral DNA in the indicated organs 21 days after infection in mice treated from day 2 after viral infection. (C) Serum anti-CL titers were determined at the indicated times; n = 8 mice, ∗P ≤ .001; 2-way ANOVA, Sidak multiple comparisons test. (D) Fluorescent PL vesicles staining of circulating B cells at day 10 after infection. PL-positive B cells were identified as CD5+CD19+CD27+CD43+ memory type B1a cells in peripheral blood and absent in NAPc2-treated mice. (E) Quantification of blood PL+ CD19+ B cells in mice treated with NAPc2 or saline control at day 10. Mean ± SD, n = 8 mice, ∗P < .0001, t test following Shapiro-Wilk test for normal distribution (F) serum anti-LBPA and anti-β2GPI titers were determined 12 weeks after infection and NAPc2 treatment for 20 days. n = 6 to 7 mice, ∗P ≤ .0001; 2-way ANOVA, Sidak multiple comparisons test.

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