Abstract
B lymphocytes play an important role in the pathophysiology of many autoimmune disorders by producing autoantibodies, secreting cytokines, and presenting antigens. B cells undergo extreme physiological changes as they develop and differentiate. Aberrant function in tolerogenic checkpoints and the metabolic state of B cells might be the contributing factors to the dysfunctionality of autoimmune B cells. Understanding B-cell metabolism in autoimmunity is important as it can give rise to new treatments. Recent investigations have revealed that alterations in metabolism occur in the activation of B cells. Several reports have suggested that germinal center (GC) B cells of individuals with systemic lupus erythematosus (SLE) have altered metabolic function. GCs are unique microenvironments in which the delicate and complex process of B-cell affinity maturation occurs through somatic hypermutation (SHM) and class switching recombination (CSR) and where Bcl6 tightly regulates B-cell differentiation into memory B-cells or plasma cells. GC B cells rely heavily on glucose, fatty acids, and oxidative phosphorylation (OXPHOS) for their energy requirements. However, the complicated association between GC B cells and their metabolism is still not clearly understood. Here, we review several studies of B-cell metabolism, highlighting the significant transformations that occur in GC progression, and suggest possible approaches that may be investigated to more precisely target aberrant B-cell metabolism in SLE.
Highlights
Received: 9 November 2021While B lymphocytes are critical cells in autoimmunity, therapeutically targeting these cells, within systemic lupus erythematosus (SLE), does not necessarily ameliorate disease [1]
These findings suggest that lupus-prone B cells are strongly linked with mTORC1-dependent enhanced metabolic activity [67,68]
The exact B-cell metabolism and signaling network in autoimmunity has not been fully elucidated, as there is a paucity of knowledge in the metabolism of Bregs, PCs, and memory
Summary
While B lymphocytes are critical cells in autoimmunity, therapeutically targeting these cells, within systemic lupus erythematosus (SLE), does not necessarily ameliorate disease [1]. In B cells, OXPHOS, glucose metabolism, fatty acid (FA) metabolism, and the citric acid cycle (TCA) are altered in SLE [6,7]. Activated T cells increase glucose metabolism in order to create enough energy and to synthesize intermediate materials for cell proliferation and differentiation [8]. Both intrinsic and extrinsic metabolic parameters regulate lymphocytes [9]. B-cell functions include antigen capture, presentation, trafficking, and antibody production, making B cells unique in function as compared to T cells These unique properties of B cells make it critical to evaluate the metabolic targets and pathways involved in immune function. T cells play a critical role in the pathogenesis of SLE, B cells play a key role in activating autoreactive T cells, contributing significantly to disease pathogenesis [9]
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