Skip to main content
. Author manuscript; available in PMC: 2014 May 1.
Published in final edited form as: Trends Pharmacol Sci. 2013 Apr 19;34(5):255–260. doi: 10.1016/j.tips.2013.03.005

Table 1.

A chart comparing the properties of 3 different chimeric mouse models is shown. The genes and type of immune deficit (adaptive and/or innate), mechanism of induction and the duration of liver injury resulting from the indicated knockout (−/−) or transgene (tg), presence of systemic toxicity, requirement for ongoing drug treatment, and selected references relating to the production of the model or use in drug metabolism are shown.

Model
 Immune
Compromise
 Liver
Injury
 Systemic
Toxicity
 Ongoing
Drug Rx
 Selected
References
uPA/SCID Adaptive (SCID) continuous uPA tg Renal Bleeding Immune Suppressive 9–12
FRG Innate (Il2rg−/−)
Adaptive (Rag2−/−) 		continuous Fah−/− None NTBC 15
TK-NOG Innate
Adaptive (Il2rg−/− SCID) 		time limited TK tg None None 18,19,20