Figure 5. Virus-specific antibodies protect against immunopathology and lead to control of virus.

C57BL/6 naïve mice were injected separately with naïve CD8⁺ T cells and non-specific antibodies (naïve serum) collected from naïve mice, and with lymphocytic choriomeningitis virus (LCMV)-specific CD8⁺ T cells and LCMV-specific antibodies (immune serum) collected from memory mice. After 2 days all mice were infected with 2 × 10⁴ plaque-forming units (PFU) of LCMV-Docile. (A) Representative immunofluorescence of spleen after 3 days of infection, stained for LCMV nucleoprotein (red) and marginal zone macrophages (CD169, green). One slide representative of 3 slides is shown. Scale bar, 200 μm. (B) Total number of LCMV-specific T cells in the spleen that were positive for the MHC class I tetramer of the glycoprotein of LCMV (Tet-GP33⁺) and for CD8 (CD8⁺) after 10 days of viral infection (n = 4–7). (C) Viral titers from spleen, inguinal LN, liver, kidney, and lungs after 10 days of viral infection (n = 7–10). (D) Levels of alanine aminotransaminase (ALT) and lactate dehydrogenase (LDH) in serum were measured after 10 days of viral infection (n = 7–10). (E) C57BL/6 mice primed with Listeria monocytogenes expressing the glycoprotein of lymphocytic choriomeningitis virus (LM-gp33) were infected with 2 × 10⁶ PFU of LCMV-Docile. After 10 days viral titers were measured in various organs, as indicated (n = 5–8). (F) C57BL/6 and B2m^−/− mice were treated with virus-specific antibodies or were left untreated. After 2 days all mice were infected with 2 × 10⁴ PFU of LCMV-Docile. Viral titers from spleen, inguinal LN, liver, kidney, and lungs were measured after 10 days of viral infection (n = 3–4). Horizontal dotted lines designate the detection limit. Data are shown as mean ± SEM and are pooled from 2 or 3 independent experiments. *P < 0.05; **P < 0.01; ***P < 0.001 (Student’s t-test).