. Author manuscript; available in PMC: 2022 Mar 15.

Published in final edited form as: J Alzheimers Dis. 2017;57(4):1123–1135. doi: 10.3233/JAD-161123

Table 3.

Selected studies on MHC-I-dependent synaptic pruning during development and neurodegeneration

Material used	Molecules investigated	Inhibitors used	Summary	References
PirB deficient mice-PirBTM mice	Mouse MHC-I receptor PirB	Genetic deletion of Pirb	Knocking out PirB in animals led to defects in eye-specific segregation and ocular dominance plasticity.	Syken, 2006 [49]
β2m/TAP1 double KO	MHC-I	Genetic deletion of cell surface MHC-I	MHC-I is expressed in neurons in the visual cortex, co-localized with postsynaptic proteins and regulated by neuronal activity.	Goddard, 2007 [48]
K^bD^b KO mice	MHC-I	Genetic deletion of MHC-I components	H2-K^b and H2-D^b can signal through neuronal MHCI receptors to enable activity-dependent remodeling of brain circuits during developmental critical periods.	Datwani, 2009 [50]
PirB−/−; APP/PS1 mice	PirB, LilrB2	Genetic deletion of PirB	LilrB2 and PirB are the receptors for Aβ oligomers and knocking out PirB in the APP/PS1 AD transgenic mice rescued not only synaptic and cognitive alterations induced in adult mice by Aβ, but also loss of plasticity during early development in visual cortex of APP/PS1 mice.	Kim, 2013 [53]
K^bD^b KO mice	MHC-I molecule H2-K^b and H2-D^b	Genetic deletion of MHC-I components	Expressing just H2-D^b in H2-K^bD^b(−/−) double knockout mice rescued defects in synapse elimination, eye-specific segregation and long-term depression (LTD).	Lee, 2014 [51]