2.6.1 JAK-STAT signaling pathway
Verena Barbarino et al 67 found that the combination of Bruton tyrosine kinase inhibitor and ibrutinib significantly reduced the antiboy-dependent cytophagocytotic effect of JAK2 on macrophages mediated, while ADCP was enhanced with JAK inhibitor or knockout of JAK2 with CRIPR Cas9. It is suggested that JAK-STAT signaling pathway can be used as a new direction in the treatment of B cell lymphoma. Furthermore, Janus kinase 2 (JAK2) was significantly absent only under ibrutinib treatment, with no significant difference in ADCP augmentation using second-generation BTKis. ADCP is a complement cascade mediated mainly by macrophages, mediated by complement receptor (CAR) and complement activator (CIC). Together with complement activation, ADCP contributes to pathogen eradication. Furthermore, JAK2 and JAK3 kinases can strengthen ADCP caused by ibrutinib.