Advances in immune-deficient mice for xenograft studies
. | Genetic background . | Rag . | IL-2rγ . | Sirpα . | c-Kit . | Human cytokines . | WT HSC . | Leukemia models . |
---|---|---|---|---|---|---|---|---|
NSG | NOD | WT | Null | NOD Sirpα | WT | None | 139 | Widely used |
NSGS | NOD | WT | Null | NOD Sirpα | WT | Transgenic hIL3/hGM-CSF/hSCF | — | AML148 ; MDS43,67 ; CML88 |
NSGW41(Wv) | NOD | WT | Null | NOD Sirpα | W41/W41 | None | 151 | — |
NBSGW | NOD | WT | Null | NOD Sirpα | W41/W41 | None | 150 | — |
C57BL/6 | ||||||||
MITRG | BALB/c | Null | Null | BALB/c Sirpα | WT | Knock-in:hIL3/ hMCSF/hTPO/hGM-CSF | 158 | Inv16/NPM1 AMLs149 |
MISTRG | BALB/c | Null | Null | Transgenic hSIRPa | WT | Knock-in:hIL3/ hMCSF/hTPO/hGM-CSF | 158 | Inv16/NPM1 AMLs149 |
. | Genetic background . | Rag . | IL-2rγ . | Sirpα . | c-Kit . | Human cytokines . | WT HSC . | Leukemia models . |
---|---|---|---|---|---|---|---|---|
NSG | NOD | WT | Null | NOD Sirpα | WT | None | 139 | Widely used |
NSGS | NOD | WT | Null | NOD Sirpα | WT | Transgenic hIL3/hGM-CSF/hSCF | — | AML148 ; MDS43,67 ; CML88 |
NSGW41(Wv) | NOD | WT | Null | NOD Sirpα | W41/W41 | None | 151 | — |
NBSGW | NOD | WT | Null | NOD Sirpα | W41/W41 | None | 150 | — |
C57BL/6 | ||||||||
MITRG | BALB/c | Null | Null | BALB/c Sirpα | WT | Knock-in:hIL3/ hMCSF/hTPO/hGM-CSF | 158 | Inv16/NPM1 AMLs149 |
MISTRG | BALB/c | Null | Null | Transgenic hSIRPa | WT | Knock-in:hIL3/ hMCSF/hTPO/hGM-CSF | 158 | Inv16/NPM1 AMLs149 |
The table provides a brief overview of the recent mouse models that have significant potential to improve the engraftment of human myeloid malignancies. Previous models are detailed in a recent review by Goyama and colleagues.147 Of note, due to high levels of cytokines, the NSGS model does not support long-term engraftment of normal hHSCs (H.M. and A. Trumpp, unpublished data). Note that both NBSGW and NSGW (W41 or Wv) lines do not require preconditioning prior to human HSC/leukemia transplantation. The NBSGW line has a mixed genetic background. MISTRG/MITRG have the advantage of expressing endogenous levels of human cytokines and are reported to engraft favorable-risk AMLs.
— , Not determined; NSG, NOD-SCIDPrkdcIL2rγ−/−; WT, wild-type.