In Vitro Diffuse Large B-Cell Lymphoma Cell Line Models as Tools to Investigate Novel Immunotherapeutic Strategies

Abstract

Despite the high incidence of diffuse large B-cell lymphoma (DLBCL), its management constitutes an ongoing challenge. The most common DLBCL variants include activated B-cell (ABC) and germinal center B-cell-like (GCB) subtypes including DLBCL with MYC and BCL2/BCL6 rearrangements which vary among each other with sensitivity to standard rituximab (RTX)-based chemoimmunotherapy regimens and lead to distinct clinical outcomes. However, as first line therapies lead to resistance/relapse (r/r) in about half of treated patients, there is an unmet clinical need to identify novel therapeutic strategies tailored for these patients. In particular, immunotherapy constitutes an attractive option largely explored in preclinical and clinical studies. Patient-derived cell lines that model primary tumor are indispensable tools that facilitate preclinical research. The current review provides an overview of available DLBCL cell line models and their utility in designing novel immunotherapeutic strategies.

Lab-on-chip technologies for exploring the gut–immune axis in metabolic disease

“…THP-1, U937) 144,145,158,159,191 and B cells (i.e. Raji, Daudi, Ramos), 192 amongst others, only a limited number of these have been used in the gut-immune lab-on-chip models under consideration. To improve models, not only is the type of immune cell or cells relevant to the research question important, whether innate or adaptive, the source of the immune cells is also an important consideration.…”

Recent Advances in IRAK1: Pharmacological and Therapeutic Aspects

“…As MYD88 functions as a signaling adaptor protein in the IRAK-dependent pathway, MYD88 mutations are most frequent in malignancies. JH-X-119-01 showed moderate cell-killing effects in these cells, with an EC 50 of 12.10 µM in the ABC-DLBCL cell line HBL-1 [24,95,96]. Additionally, as BTK inhibition has been previously shown to synergize with IRAK inhibition, JH-X-119-01 was co-treated with the BTK inhibitor ibrutinib, which showed synergistic tumor cell-killing effects in MYD88mutated B-cell lymphoma cells [35].…”