The effect of ibrutinib on the myeloid cell compartment in CNS lymphoma

The Bruton’s tyrosine kinase inhibitor (BTKi) ibrutinib effectively blocks downstream B-cell receptor activation and has demonstrated clinical efficacy both as monotherapy and in combination with immunochemotherapy in patients with central nervous system lymphoma (CNSL) [ 1 , 2 ]. Beyond its direct effect on lymphoma cells, ibrutinib regulates the tumor microenvironment (TME) and enhances T-cell immunity and function in systemic B-cell Non-Hodgkin lymphomas (NHL) such as chronic lymphocytic leukemia (CLL) [ 3 , 4 ]. However, its impact on the tumor immune landscape of B-cell lymphomas within immune-privileged sites like the CNS remains largely unexplored, primarily due to challenges associated with the availability of appropriate CNS lymphoma tissue following ibrutinib treatment.