| First Author | Sam H | Year | 1999 |
| Journal | Infect Immun | Volume | 67 |
| Issue | 5 | Pages | 2660-4 |
| PubMed ID | 10225939 | Mgi Jnum | J:55976 |
| Mgi Id | MGI:1339841 | Doi | 10.1128/iai.67.5.2660-2664.1999 |
| Citation | Sam H, et al. (1999) Deficiency in tumor necrosis factor alpha activity does not impair early protective Th1 responses against blood-stage malaria. Infect Immun 67(5):2660-4 |
| abstractText | Blood-stage Plasmodium chabaudi AS infection was controlled by 4 weeks in mice with deletion of tumor necrosis factor p55 and p75 receptors (TNFR-knockout [KO]) and control wild-type (WT) mice, although female TNFR-KO mice showed slightly but significantly higher parasitemia immediately following the peak. Serum interleukin 12 (IL-12) p70 and gamma interferon (IFN-gamma) levels were similar but tumor necrosis factor alpha levels were significantly higher in TNFR-KO mice than in WT controls. Splenic IL-12 receptor beta1 and beta2 and IFN-gamma mRNA expression, as well as spleen cell production of IFN-gamma and IL-4, were comparable in both mouse types, but IL-10 production was significantly higher in cells from TNFR-KO mice than in cells from WT mice. Lipopolysaccharide-induced NO secretion by splenic macrophages in vitro was significantly reduced but systemic NO3- levels were similar in infected TNFR-KO and WT mice. |
