| First Author | Vogel SN | Year | 1999 |
| Journal | J Immunol | Volume | 162 |
| Issue | 10 | Pages | 5666-70 |
| PubMed ID | 10229796 | Mgi Jnum | J:54987 |
| Mgi Id | MGI:1336850 | Doi | 10.4049/jimmunol.162.10.5666 |
| Citation | Vogel SN, et al. (1999) Cutting edge: functional characterization of the effect of the C3H/HeJ defect in mice that lack an Lpsn gene: in vivo evidence for a dominant negative mutation. J Immunol 162(10):5666-70 |
| abstractText | A point mutation in the Tlr4 gene, which encodes Toll-like receptor 4, has recently been proposed to underlie LPS hyporesponsiveness in C3H/HeJ mice (Lps(d)), The data presented herein demonstrate that F-1 progeny from crosses between mice that carry a similar to 9-cM deletion of chromosome 4 (including deletion of Lps(Tlr4)) and C3H/HeJ mice (i.e., Lps(0) x Lps(d) F-1 mice) exhibit a pattern of LPS sensitivity, measured by TNF activity, that is indistinguishable from that exhibited by Lps(n) x Lps(d) F- 1 progeny and whose average response is ''intermediate'' to parental responses. Thus, these data provide clear functional support for the hypothesis that the C3H/HeJ defect exerts a dominant negative effect on LPS sensitivity; however, expression of a normal Toll-like receptor 4 molecule is apparently not required. |
