Figure 7.
Figure 7. SAP– immunopathology is CD8 T-cell mediated. SAP– mice and SAP– mice depleted of CD8 T cells (SAP– + anti-CD8) were infected with 4 × 106 PFU LCMVcl13 and examined for immunopathology. (A) Clinical illness. Mice were examined visually and assigned a composite score based on signs of illness (ruffled fur, mobility, hunched back; maximum possible score, 9; normal health, 0). CD8-depleted SAP– mice were significantly healthier than normal SAP– mice (P < .001) (left panel); n indicates uninfected, naive control mouse. Clinical disease was also ameliorated in WT mice depleted of CD8 T cells, as expected (right panel). SAP–,n = 4; SAP– + anti-CD8; n = 4; WT, n = 4; WT + anti-CD8, n = 4; naives, n = 2. (B) Body weight 1 week after infection. Weight loss was significantly worse in normal SAP– mice than in CD8-depleted SAP– mice (P < .01). (C) Spleen histology day 8 after infection. Sections were fixed in formalin and then counterstained with hematoxylin and eosin. A representative white pulp region is shown for SAP– and SAP– + anti-CD8 tissue sections (top panels). Extensive disruption of the white pulp and splenic architecture is present in SAP– mice, in contrast with SAP– mice treated with anti-CD8 antibody. Bottom panels show sections from treated and untreated WT mice infected with LCMVcl13. (D) Spleen cell counts day 8 after infection. Spleens from intact SAP– mice were significantly smaller and more acellular than spleens from CD8-depleted SAP– mice (P < .01). (E) Lymph node (axillary) cell counts day 8 after infection. (F) Wild-type spleen cell counts day 8 after infection. All data are representative of 3 independent experiments. *P < .05. **P < .01. ***P < .001.

SAP immunopathology is CD8 T-cell mediated.SAP mice and SAP mice depleted of CD8 T cells (SAP + anti-CD8) were infected with 4 × 106 PFU LCMVcl13 and examined for immunopathology. (A) Clinical illness. Mice were examined visually and assigned a composite score based on signs of illness (ruffled fur, mobility, hunched back; maximum possible score, 9; normal health, 0). CD8-depleted SAP mice were significantly healthier than normal SAP mice (P < .001) (left panel); n indicates uninfected, naive control mouse. Clinical disease was also ameliorated in WT mice depleted of CD8 T cells, as expected (right panel). SAP,n = 4; SAP + anti-CD8; n = 4; WT, n = 4; WT + anti-CD8, n = 4; naives, n = 2. (B) Body weight 1 week after infection. Weight loss was significantly worse in normal SAP mice than in CD8-depleted SAP mice (P < .01). (C) Spleen histology day 8 after infection. Sections were fixed in formalin and then counterstained with hematoxylin and eosin. A representative white pulp region is shown for SAP and SAP + anti-CD8 tissue sections (top panels). Extensive disruption of the white pulp and splenic architecture is present in SAP mice, in contrast with SAP mice treated with anti-CD8 antibody. Bottom panels show sections from treated and untreated WT mice infected with LCMVcl13. (D) Spleen cell counts day 8 after infection. Spleens from intact SAP mice were significantly smaller and more acellular than spleens from CD8-depleted SAP mice (P < .01). (E) Lymph node (axillary) cell counts day 8 after infection. (F) Wild-type spleen cell counts day 8 after infection. All data are representative of 3 independent experiments. *P < .05. **P < .01. ***P < .001.

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