PTPN22 and islet-specific autoimmunity: What have the mouse models taught us?

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 background	Spontaneous autoimmunity1	AAbs	T1D	B cells	T cells	Ref.
PTPN22 knock-out	C57BL/6	No	No	No	intact	↑Memory/effector number ↑Treg number and function ↑TFH number and function ↑Tr1 number and function	[72-75,84]
PTPN22 knock-out	RIP-LCMV (B6)	No	No	Exacerbated	Not examined	↑Effector function	[81]
PTPN22 R619W knock-in	C57BL/6	No	No	No	Not examined	↑Memory/effector number	[68]
PTPN22 R619W knock-in	C57BL/6 x 129	Lupus-like disease	Yes	No	↑Transitional and Self-reactive	↑Memory/effector number	[67]
PTPN22 R619W transgenic	C57BL/6	No	No	No	Not examined	No differences	[77]
PTPN22 knock-down	NOD	No	No	Protected	↑Activation	↑Treg number and function	[78]
PTPN22 transgenic	NOD	No	No	Protected	Not examined	↓Memory/effector number	[79]
PTPN22 R619W knock-in	NOD	No	↑↑	Exacerbated	Not examined	Not examined	[76]

¹Other than T1D. T1D: Type 1 diabetes; AAbs: Autoantibodies; Treg: T regulatory cell; PTPN22: Protein tyrosin phosphatase non-receptor 22; TFH: T follicular helper.