Abstract
Since its discovery in 1968 by Sultzer (1) as a mutant mouse strain which displayed aberrant peritoneal inflammatory cell responses to endotoxin, the C3H/HeJ mouse has served as one of the dominant experimental models by which to define both in vivo and in vitro the mode of action of endotoxin. Extensive studies have documented that the phenotypic characteristic of endotoxin unresponsiveness is specific for the LPS fraction of endotoxin, and more specifically, the lipid A component (reviewed in 2). Further, the available evidence would suggest that the defect responsible for LPS/lipid A unresponsiveness may be a characteristic of all cells derived from this mouse in that lymphocytes, macrophages and fibroblasts are all refractory to LPS stimulation (3). Genetic evidence has clearly linked this mutation to a locus on chromosome 4. This locus appears to be codominantly expressed and LPS unresponsiveness is inherited as a single gene trait in the appropriate F2 backcrosses (5).
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References
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Morrison, D.C., Wollenweber, HW., Vukajlovich, S.W., Goodman, S.A. (1986). Biochemical, Immunological and Functional Analysis of Lymphocytes from the LPS-Non-Responder C3H/HeJ Mouse. In: Szentivanyi, A., Friedman, H., Nowotny, A. (eds) Immunobiology and Immunopharmacology of Bacterial Endotoxins. University of South Florida International Biomedical Symposia Series, vol 18. Springer, Boston, MA. https://doi.org/10.1007/978-1-4613-2253-5_28
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DOI: https://doi.org/10.1007/978-1-4613-2253-5_28
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