Figure 1.
Deletion of Ccl3-producing cells aggravates mCMV infection. (A) Schematic representation of knock-in construct designed to tag endogenous Ccl3 with Venus, report of Ccl3 promotor activity via tdTomato expression, and DTR-mediated deletion of Ccl3-expressing cells. (B) Scheme of the experiment. C57BL6/J (BL6) and CCL3-EASER mice were treated with DT or PBS. 1 day later, mice were infected with mCMV and analyzed at the indicated time points. (C) Representative contour (left) and dot plots (right) of liver-associated leukocytes of CCL3-EASER mice treated as indicated. 1 day later, liver leukocytes were analyzed by flow cytometry. (D) Quantification of C. (E) Viral load of PBS- or DT-treated CCL3-EASER and BL6 mice 4 and 7 days after infection. (F) Bright-field microscopy images showing 8 µm liver sections stained with mAB Croma101 directed against mCMV IE1 4 days after infection. Red arrowheads indicate mCMV positive cells. Scale bar 50 µm. (G) Histopathological evaluation of paraffin-embedded liver tissue sections stained with hematoxylin-eosin 4 days after mCMV infection. Red arrowheads indicate immune infiltration. Scale bar 100 µm. Images were acquired as tile scans with 20× magnification and automatic stitching with 5% overlap using ZEN Blue software. Data in D–E are presented as mean ± SD. Each symbol represents individual mice. Shown is one representative of at least two independent experiments. Statistical difference was assessed by unpaired nonparametric Mann–Whitney U-test: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Data in D–F are representative of three mice per group of two independent experiments. n.s. stands for not statistically significant; d.p.i., days post infection; CV, central vein; PV, portal vein.

Deletion of Ccl3-producing cells aggravates mCMV infection. (A) Schematic representation of knock-in construct designed to tag endogenous Ccl3 with Venus, report of Ccl3 promotor activity via tdTomato expression, and DTR-mediated deletion of Ccl3-expressing cells. (B) Scheme of the experiment. C57BL6/J (BL6) and CCL3-EASER mice were treated with DT or PBS. 1 day later, mice were infected with mCMV and analyzed at the indicated time points. (C) Representative contour (left) and dot plots (right) of liver-associated leukocytes of CCL3-EASER mice treated as indicated. 1 day later, liver leukocytes were analyzed by flow cytometry. (D) Quantification of C. (E) Viral load of PBS- or DT-treated CCL3-EASER and BL6 mice 4 and 7 days after infection. (F) Bright-field microscopy images showing 8 µm liver sections stained with mAB Croma101 directed against mCMV IE1 4 days after infection. Red arrowheads indicate mCMV positive cells. Scale bar 50 µm. (G) Histopathological evaluation of paraffin-embedded liver tissue sections stained with hematoxylin-eosin 4 days after mCMV infection. Red arrowheads indicate immune infiltration. Scale bar 100 µm. Images were acquired as tile scans with 20× magnification and automatic stitching with 5% overlap using ZEN Blue software. Data in D–E are presented as mean ± SD. Each symbol represents individual mice. Shown is one representative of at least two independent experiments. Statistical difference was assessed by unpaired nonparametric Mann–Whitney U-test: *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Data in D–F are representative of three mice per group of two independent experiments. n.s. stands for not statistically significant; d.p.i., days post infection; CV, central vein; PV, portal vein.

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