Table 1.
The role of IL-12 in sustaining production of IFN-γ production in wild-type and IL-12−/− BALB/c mice after infection with L. major
| IFN-γ, pg/ml
|
||
|---|---|---|
| Media | SLA | |
| Week 1 post-infection | ||
| Wild-type mice plus IL-12 (5 days) | <300 | 5,822 ± 349 |
| IL-12−/− mice plus IL-12 (5 days) | <300 | 4,546 ± 227 |
| Week 6 post-infection | ||
| Wild-type mice | <300 | <300 |
| Wild-type mice plus IL-12 (5 days) | <300 | 2,076 ± 72 |
| IL-12−/− mice | <300 | <300 |
| IL-12−/− mice plus IL-12 (5 days) | <300 | <300 |
| IL-12−/− mice plus IL-12 (5 days plus weekly) | <300 | 1,666 ± 49 |
Groups of wild-type BALB/c or IL-12−/− mice (n = 8 per group) were infected with L. major and were treated with IL-12 (1 μg) at the time of infection (day 0) and for the following 4 days for a total treatment of 5 days. A group of IL-12−/− mice initially treated with IL-12 for 5 days was given supplemental treatment with rIL-12 (1 μg) i.p. once a week for the following 5 weeks. Pooled lymph nodes were harvested from groups of mice (n = 4) either 1 week or 6 weeks post-infection. Single-cell suspensions of total lymph node cells (3 × 105 cells/well) were stimulated in vitro in a 96-well microtiter plate in the presence of absence of 25 μg/ml of soluble leishmania antigen (SLA). Culture supernatants were harvested after 48 h, and production of IFN-γ was assessed by ELISA. The lower limit of detection for IFN-γ was 100–300 pg/ml. The standard error of the mean was <10%.