Metabolic Program of Regulatory B Lymphocytes and Influence in the Control of Malignant and Autoimmune Situations

Metabolic pathways have been studied for a while in eukaryotic cells. During glycolysis, glucose enters into the cells through the Glut1 transporter to be phosphorylated and metabolized generating ATP molecules. Immune cells can use additional pathways to adapt their energetic needs. The pentose phosphate pathway, the glutaminolysis, the fatty acid oxidation and the oxidative phosphorylation generate additional metabolites to respond to the physiological requirements. Specifically, in B lymphocytes, these pathways are activated to meet energetic demands in relation to their maturation status and their functional orientation (tolerance, effector or regulatory activities). These metabolic programs are differentially involved depending on the receptors and the co-activation molecules stimulated. Their induction may also vary according to the influence of the microenvironment, i.e. the presence of T cells, cytokines horizontal ellipsis promoting the expression of particular transcription factors that direct the energetic program and modulate the number of ATP molecule produced. The current review provides recent advances showing the underestimated influence of the metabolic pathways in the control of the B cell physiology, with a particular focus on the regulatory B cells, but also in the oncogenic and autoimmune evolution of the B cells.

Automated summary

Cells have multiple pathways to fulfill their energetic needs, with the activation of metabolic pathways depending on various factors such as microenvironment, cell receptors, and co-activation molecules. The influence of the microenvironment and the expression of specific transcription factors play a crucial role in directing the energetic program and modulating the production of ATP molecules. The study underscores the significant impact of metabolic pathways on the control of B cell physiology, particularly in regulatory B cells, oncogenic progression, and autoimmune evolution.