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.