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Copyright ©The Author(s) 2017.
World J Diabetes. Jul 15, 2017; 8(7): 330-336
Published online Jul 15, 2017. doi: 10.4239/wjd.v8.i7.330
Table 1 Summary of mouse models where the role of protein tyrosin phosphatase non-receptor 22 in type 1 diabetes incidence has been directly or indirectly addressed
Genetic backgroundSpontaneous autoimmunity1AAbsT1DB cellsT cellsRef.
PTPN22 knock-outC57BL/6NoNoNointact↑Memory/effector number ↑Treg number and function ↑TFH number and function ↑Tr1 number and function[72-75,84]
PTPN22 knock-outRIP-LCMV (B6)NoNoExacerbatedNot examined↑Effector function[81]
PTPN22 R619W knock-inC57BL/6NoNoNoNot examined↑Memory/effector number[68]
PTPN22 R619W knock-inC57BL/6 x 129Lupus-like diseaseYesNo↑Transitional and Self-reactive↑Memory/effector number[67]
PTPN22 R619W transgenicC57BL/6NoNoNoNot examinedNo differences[77]
PTPN22 knock-downNODNoNoProtected↑Activation↑Treg number and function[78]
PTPN22 transgenicNODNoNoProtectedNot examined↓Memory/effector number[79]
PTPN22 R619W knock-inNODNo↑↑ExacerbatedNot examinedNot examined[76]