Abstract
The interplay between the immune system and the metabolic state of a cell is intricate. In all phases of an immune response, the corresponding metabolic changes shall occur to support its modulation, in addition to the signalling through the cytokine environment and immune receptor stimulation. While autoimmune disorders may develop because of a metabolic imbalance that modulates switching between T‐cell phenotypes, the effects that the interaction between T and B cells have on one another's cellular metabolism are yet to be understood in disease context. Here, we propose a perspective which highlights the potential of targeting metabolism to modulate T‐ and B‐cell subtypes populations as well as T–B and B–T cell interactions to successfully treat autoimmune disorders. Specifically, we envision how metabolic changes can tip the balance of immune cells interactions, through definite mechanisms in both health and disease, to explain phenotype switches of B and T cells. Within this scenario, we highlight targeting metabolism that link inflammation, immunometabolism, epigenetics and ageing, is critical to understand inflammatory disorders. The combination of treatments targeting immune cells that cause (T/B) cell phenotype imbalances, and the metabolic pathways involved, may increase the effectiveness of treatment of autoimmune disorders, and/or ameliorate their symptoms to improve patients’ quality of life.
Metabolic imbalance underlies development of autoimmune disorders.
Metabolic changes modulate switching between immune cell phenotypes.
Targeting metabolism regulates T–B and B–T cell interactions.
Ageing at the interface between autoimmune disorders and metabolic syndromes.
Conceptual scheme of T–B and B–T cell interactions at the metabolic level. The mutual modulation of metabolic pathways between T and B cells favours an increased metabolic activity, generating feedback of activation. T cells can affect B‐cell metabolism and B cells can affect T‐cell metabolism, through the signalling pathways triggered both by receptor stimulation and cytokine release. Through mutual regulation, T and B cells can meet the metabolic demand required in each stage of their development and differentiate to a specific phenotype.