Epigenetic dysregulation of B‑cells in autoimmune diseases and lymphomas (Review)

B‑lymphocytes (B‑cells) develop from hematopoietic stem cells in the bone marrow or fetal liver and differentiate into antibody‑secreting cells and memory B‑cells upon encountering antigens in peripheral lymphoid organs. Throughout this process, the expression of lineage‑associated genes is upregulated, whereas that of lineage‑inappropriate genes is repressed, thereby directing commitment to a specific B‑cell fate. Epigenetic regulatory mechanisms, including DNA methylation, post‑translational histone modifications and non‑coding RNAs, regulate gene transcription and play crucial roles in B‑cell development and differentiation. The dysregulation of these epigenetic processes may contribute to the pathogenesis of autoimmune diseases and B‑cell malignancies. Recent advances in high‑throughput techniques, including single‑cell RNA sequencing, chromatin immunoprecipitation‑sequencing and whole‑genome bisulfite sequencing, have significantly enhanced the understanding of epigenetic dysregulation in these disorders. The present review summarizes recent advances in the understanding of dysregulated epigenetic mechanisms underlying B‑cell‑mediated autoimmune diseases (such as systemic lupus erythematosus, rheumatoid arthritis, primary Sjögren's syndrome, multiple sclerosis and type 1 diabetes mellitus) and lymphomas (such as diffuse large B‑cell lymphoma, follicular lymphoma, mantle cell lymphoma, Burkitt lymphoma and marginal zone lymphoma), and highlights emerging diagnostic biomarkers and therapeutic strategies.