Fig. 3
From: Bruton tyrosine kinase inhibitors in B-cell lymphoma: beyond the antitumour effect
When fungal infection happens, neutrophils was recruited to the sites of inflammation by cytokines and then release granule proteins and reactive oxygen. BTKis seem to block their release. Additionally, BTK plays a crucial role in neutrophils development and maturation, which can also be inhibited by BTKis. Macrophages also mediate the recruitment of neutrophils by releasing IL1β and TNFα. In addition, macrophages can eliminate fungus by phagocytosis. TLR2/4 and Dectin-1 can recognize β-glucans, chitins and mannans (PAMPs) of fungus and then induce downstream signaling cascades via BTK including NFκB and nuclear factor of activated T-cells (NFAT). However, BTKi not only impair the phagocytosis of macrophages, but also inhibit cytokine release and disrupt the signal transduction