CO72 | CK2 drives immune cell recruitment via cytokine modulation in Hodgkin lymphoma

Introduction: Classic Hodgkin Lymphoma (cHL) is characterized by a small population of malignant Hodgkin and Reed–Sternberg (HRS) cells that shape the tumor microenvironment (TME) via cytokines and chemokines secretion. These factors drive immune cells recruitment and establish an immunosuppressive milieu supporting neoplastic cells survival. The molecular basis of this aberrant secretory phenotype remains largely unknown. We recently identified the kinase CK2 as a critical regulator of cHL cell survival, whose inhibition induces apoptosis. Given CK2 involvement in signaling pathways controlling inflammation and cell migration, this study investigates its contribution to TME modulation in cHL.Methods: cHL cell lines (HDLM-2, KM-H2, L-428, and L-540) were treated with 0, 5, or 10 µM of the CK2 inhibitor CX-4945 (CX) for 24 or 48h. Migration assays were performed using T and B cells purified from healthy donors in fibronectin-coated transwells. Conditioned media (CM) from treated cHL cells was placed in the lower chambers. Migrated lymphocytes were quantified by flow cytometry. Cytokine levels in cHL supernatants after 24h of treatment were analyzed using a 25-plex array and validated by ELISA or by an Automated Immunoassay System for multiplex ELISA (ELLA). Results: Our results revealed that CM from cHL cell lines showed a reduced chemoattractant effect on T and B cells when CK2 was inhibited by CX. T-cell migration toward CM from HDLM-2, KM-H2, L-428, and L-540 cells after 24h of treatment with 5 µM CX decreased by 12.1%, 18%, 30.2%, and 8.2% respectively (p