| First Author | McLeod R | Year | 1984 |
| Journal | J Infect Dis | Volume | 149 |
| Issue | 2 | Pages | 234-44 |
| PubMed ID | 6699433 | Mgi Jnum | J:39992 |
| Mgi Id | MGI:87331 | Doi | 10.1093/infdis/149.2.234 |
| Citation | McLeod R, et al. (1984) Immune response of mice to ingested Toxoplasma gondii: a model of toxoplasma infection acquired by ingestion. J Infect Dis 149(2):234-44 |
| abstractText | SWR/J mice perorally infected with the Me49 strain of Toxoplasma gondii developed thymic cortical atrophy, clusters of epithelioid cells and plasma cells in lymphoid tissue, and hepatic inflammation during the first month after infection; the inflammation subsequently decreased. Antibody to T gondii was present in serum on day 14 after infection, reached a maximal titer by one month, and remained at this titer for five months. Splenic lymphocyte blastogenesis in response to concanavalin A was depressed for one month but returned to normal in most mice by two months. Splenic lymphocyte blastogenesis in response to toxoplasma antigens (stimulation index, greater than or equal to 1.6) developed in one-third of mice after two months of infection but did not develop in others even after five months of infection. Peritoneal macrophages had an enhanced microbicidal capacity against T gondii from 14 days until five months after infection. Peroral administration of the Me49 strain of T gondii was lethal for Beige-C57BL/6J and C57BL/6J mice; these strains of mice showed the most extensive changes, necrosis, thrombi, and many trophozoites in tissues. |
