“…The alternative concept, namely agonizing immune inhibitory checkpoints, to treat AID has also been proposed in the literature in the past years (63, [98][99][100][101][102] and the efficacy of several coinhibitory agonists has been demonstrated preclinically in vitro using human peripheral blood mononuclear cells (PBMC) and in vivo using rodent models of AID (103)(104)(105)(106). Among others, B-and T-lymphocyte attenuator (BTLA/CD272) (107), lymphocyte-activation gene 3 (LAG-3/CD223) (107,108), T cell immunoglobulin and mucin-domain containing-3 (TIM-3) (107,108), T cell immunoreceptor with Ig and ITIM domains (TIGIT) (107)(108)(109)(110)(111)(112)(113)(114), PD1/PD-L1 (63, 101) and V-domain Ig suppressor of T cell activation (VISTA) (107,115,116) are emerging as very attractive target candidates for agonistic immune checkpoint intervention in AID.…”