CD8A and acute myeloid leukemia: LILRB3 antibody agonism of AML cells promoted the expression of immunoinhibitory markers including IL10 and CD163 [21].The pro-survival benefit of anti-LILRB3 antibodies observed in humanized mice was of CD8 T-cells abolished the pro-survival effects of anti-LILRB3 antibodies significantly but not completely abrogated with CD8 depletion, highlighting the crucial contribution immune inhibition plays in LILRB3 mediated pathogenesis [53].