The expression of LILRB2/PirB in patients with intractable TLE and model mice was dramatically increased, respectively.
The downstream molecules of LILRB2/PirB have been activated in the epileptic foci of TLE patients.
LILRB2/PirB and its downstream factors are highly expressed in neurons and astrocytes.
The protein levels of LILRB2 negatively correlated with the frequency of seizures in TLE patients.