DLBCL is a testament to the complexity of nature. It is characterized by remarkable diversity in its molecular and pathological subtypes and clinical manifestations. Despite the strides made in DLBCL treatment and the introduction of innovative drugs, around one-third of patients face a relapse or develop refractory disease. Recent findings over the past ten years have highlighted the critical interplay between the evolution of DLBCL and various epigenetic mechanisms, including chromatin remodeling, DNA methylation, histone modifications, and the regulatory roles of non-coding RNAs. These epigenetic alterations are integral to the pathways of oncogenesis, tumor progression, and the development of therapeutic resistance. In the past decade, the identification of dysregulated epigenetic mechanisms in lymphomas has paved the way for an exciting field of epigenetic therapies. Crucially, these epigenetic transformations span beyond tumor cells to include the sophisticated network within the tumor microenvironment (TME). While the exploration of epigenetic dysregulation in lymphoma cells is thriving, the mechanisms affecting the functions of immune cells in the TME invite further investigation. This review is dedicated to weaving together the narrative of epigenetic alterations impacting both lymphoma cells with a focus on their infiltrating immune companions.

Introduction: About one in four people show an immunological reaction to an infection with Mycobacterium tuberculosis, which can remain latent or lead to active forms of the disease. Psoriasis is a chronic, immune-mediated skin disease that can be associated with numerous comorbidities. Biologic therapies have revolutionized psoriasis treatment but carry the risk of reactivating latent tuberculosis infection. However, the link between tuberculosis as a triggering factor for the onset of psoriasis remains unknown. Clinical Case: We present the case of a patient initially diagnosed with secondary pulmonary tuberculosis, who, two months after the diagnosis, showed a remarkable clinical evolution by developing lesions consistent with vulgar psoriasis, necessitating a multidisciplinary treatment approach. Discussions: This unique case highlights the shared immune mechanism of these diseases, particularly involving TNF-α, IL-17, and CD4+ T cells. Conclusions: The coexistence of these conditions raises critical questions about the interplay between infectious and autoimmune diseases and the impact of genetic susceptibility.