| First Author | Honma N | Year | 2000 |
| Journal | Immunology | Volume | 100 |
| Issue | 1 | Pages | 84-90 |
| PubMed ID | 10809963 | Mgi Jnum | J:75496 |
| Mgi Id | MGI:2176690 | Doi | 10.1046/j.1365-2567.2000.00011.x |
| Citation | Honma N, et al. (2000) Deficiency of the macrophage migration inhibitory factor gene has no significant effect on endotoxaemia. Immunology 100(1):84-90 |
| abstractText | By targeted disruption of the MIF gene, we have established a mouse strain deficient in macrophage (Mphi) migration inhibitory factor (MIF). Despite previous reports indicating an essential role of MIF in endotoxaemia, an injection of lipopolysaccharide (LPS) into the MIF-deficient mice (maintained under specific pathogen-free conditions) caused shock. No significant difference was detected between the MIF-deficient mutant and normal mice in susceptibility to LPS for endotoxaemia or tumour necrosis factor-alpha (TNF-alpha) formation upon LPS injection. Peritoneal Mphi from the two strains produced TNF-alpha in response to LPS with similar dose responses. Dexamethasone suppressed the LPS-induced TNF-alpha response of Mphi, but no difference was detected between the Mphi from the two strains. These results suggest that endogenous MIF has no significant effect on the LPS-induced TNF-alpha production and no effect on suppression of the response by glucocorticoids. Thus, MIF is not crucial for LPS-induced immune responses leading to shock. |
