TABLE 1.
Effect of depleting γδ+ T cells on CVB3-induced myocarditisa
| Strain | Antibody treatment | Cumulative mortality (day 7) | Mean virus titer (log 10 PFU) ± SEM | % Myocardium inflamed (mean ± SEM) |
|---|---|---|---|---|
| C57BL/6 (IA+ IE−) | None | 0 | 5.1 ± 0.7 | 0.5 ± 0.3 |
| Anti-γδ TcR | 0 | 5.5 ± 0.9 | 0 ± 0 | |
| ABo (IA− IE−) | None | 0 | 6.5 ± 1.4 | 0 ± 0 |
| Anti-γδ TcR | 0 | 7.1 ± 0.8 | 1.3 ± 0.8 | |
| ABoEαk (IA− IE+) | None | 100 | 6.2 ± 0.9 | 5.1 ± 2.0b |
| Anti-γδ TcR | 25 | 6.5 ± 0.7 | 1.8 ± 1.1c | |
| BL.Tg.Eαk (IA+ IE+) | None | 50 | 4.3 ± 0.5 | 8.3 ± 1.6b |
| Anti-γδ TcR | 0 | 5.3 ± 0.4c | 1.7 ± 0.5bc |
Male mice, 4 to 5 weeks of age, were injected i.p. with 100 μg of GL3-3A (anti-γδ) monoclonal antibody in 0.5 ml of PBS or isotype hamster IgG on days −1 and −2 relative to virus infection. Animals received 5 × 7 104 PFU of CVB3 on day 0, and surviving animals were euthanized on day 7. Hearts were removed from animals dying between days 5 and 7 for analysis. Hearts were divided, and the apex was formalin fixed, sectioned, and evaluated by image analysis for percentage of myocardium affected. The remaining tissue was titered by plaque-forming assay for virus. Groups consisted of four mice each.
Significantly different from C57BL/6 at P ≤ 0.05.
Significantly different from non-antibody-treated mice at P ≤ 0.05 by Wilcoxon ranked score.