Oxidative Stress and Inflammation in B-Cell Lymphomas

Abstract

Mature lymphoid neoplasms arise de novo or by the transformation of more indolent lymphomas in a process that relies on the stepwise accumulation of genomic and transcriptomic alterations. The microenvironment and neoplastic precursor cells are heavily influenced by pro-inflammatory signaling, regulated in part by oxidative stress and inflammation. Reactive oxygen species (ROSs) are by-products of cellular metabolism able to modulate cell signaling and fate. Moreover, they play a crucial role in the phagocyte system, which is responsible for antigen presentation and the selection of mature B and T cells under normal conditions. Imbalances in pro-oxidant and antioxidant signaling can lead to physiological dysfunction and disease development by disrupting metabolic processes and cell signaling. This narrative review aims to analyze the impact of reactive oxygen species on lymphomagenesis, specifically examining the regulation of microenvironmental players, as well as the response to therapy for B-cell-derived non-Hodgkin lymphomas. Further research is needed to investigate the involvement of ROS and inflammation in the development of lymphomas, which may unravel disease mechanisms and identify innovative therapeutic targets.

Unveiling the micronutrient‐immunity puzzle in inactivated COVID‐19 vaccination: A comprehensive analysis of circulating micronutrient levels and humoral responses in healthy adults

“…Elevated blood iron and zinc concentrations were inversely associated with the binding affinity of anti‐SARS‐CoV‐2 IgM antibodies, suggesting a potential dampening effect on early humoral responses. This finding aligns with existing evidence linking iron dysregulation to oxidative stress and pro‐inflammatory pathways, 30 known to impair B‐cell function 31 . Additionally, studies in animal models have linked iron overload with pulmonary fibrosis 32 and inhibit the activity and differentiation of T helper cells, 33 which regulate B‐cell proliferation and antibody production through cytokine modulations 34 .…”

“…This finding aligns with existing evidence linking iron dysregulation to oxidative stress and pro-inflammatory pathways, 30 known to impair B-cell function. 31 Additionally, studies in animal models have linked iron overload with pulmonary fibrosis 32 and inhibit the activity and differentiation of T helper cells, 33 which regulate B-cell proliferation and antibody production through cytokine modulations. 34 These observations collectively suggest that iron could exacerbate viral infection and hinder humoral responses in COVID-19 at certain concentrations.…”

Effect of Diet and Oxidative Stress in the Pathogenesis of Lymphoproliferative Disorders

“…Confirming with the above report that the presence of genetic aberrations, in the absence of interactions with the environment, are not sufficient to result in complete malignant transformation of the cell [137], several general population studies have shown that some translocations, such as t (14,18), are also present in lymphocytes from individuals without lymphoproliferative disorders [138].…”

“…It has been seen that the polymorphism (Ser608Leu) of the NOS2A gene, which codes for inducible nitric oxide synthase (iNOS), determines a greater enzymatic activity and subsequent increase in nitric oxide (NO) [ 144 ]; this polymorphism has been found in many cases of NHL, particularly in subtypes DLBCL and FL. Moreover, a statistically significant association has been identified between B-cell lymphomas and the polymorphism of manganese superoxide dismutase (SOD2 Val16Ala) [ 137 , 143 ]. Other studies have demonstrated an association between NHL and myeloperoxidase (MPO) and glutathione peroxidase (GPX1) polymorphisms; a correlation was seen between FL and MPO (642G > A) and between marginal zone B-cell lymphoma (MZL) and GPX1 (Ex1-226C > T) [ 145 , 146 ].…”

Disturbed Plasma Lipidomic Profiles in Females with Diffuse Large B-Cell Lymphoma: A Pilot Study

“…The role of the AA pathway and inflammation in the pathogenesis and progression of B-cell lymphomas including DLBCL has been increasingly recognised [78]. Interestingly, while tumour cells derived from 85% of Hodgkin lymphomas expressed 15-LOX 1, the enzyme was not detected in any of the ten biopsies that represented nine different subtypes of NHL, which makes 15-LOX 1 a candidate biomarker to distinguish Hodgkin from NHL [79].…”