Skip to main content
Fig. 4 | Experimental Hematology & Oncology

Fig. 4

From: Bruton tyrosine kinase inhibitors in B-cell lymphoma: beyond the antitumour effect

Fig. 4

When SARS-CoV2 enters the respiratory tract and causes an infection, alveolar macrophages may engulf viral particles or cellular debris. Viral single-stranded RNA (ssRNA) binds to Toll-like receptor7/8 (TLR7/8) and then activates Bruton tyrosine kinase (BTK) and myeloid differentiation primary response 88 (MYD88). For one thing, activation of the BTK-dependent nuclear factor kappa B (NF-κB) pathway leads to the production of a series of pro-inflammatory factors and chemokines, which are called cytokine storms. Among these, IL-8 can recruit more neutrophils in the late phase of severe coronavirus disease 2019(COVID-19 infection. BTKi can inhibit TLR-dependent NF-κB signaling pathway, thereby preventing cytokine production. For another, during severe COVID-19, the accumulated NLR family pyrin domain containing 3(NLRP3)inflammasome is phosphorylated by BTK, thus promoting its oligomerization and assembly into an inflammasome (pro-IL-1β to mature IL-1β). BTKis inhibit inflammasome-mediated process

Back to article page