Metabolic imbalance driving immune cell phenotype switching in autoimmune disorders: Tipping the balance of T‐ and B‐cell interactions

Author:

Barberis Matteo123ORCID,Rojas López Alejandra12ORCID

Affiliation:

1. Molecular Systems Biology School of Biosciences Faculty of Health and Medical Sciences University of Surrey Guildford Surrey UK

2. Centre for Mathematical and Computational Biology, CMCB University of Surrey Guildford Surrey UK

3. Synthetic Systems Biology and Nuclear Organization Swammerdam Institute for Life Sciences University of Amsterdam Amsterdam The Netherlands

Abstract

AbstractThe 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.

Publisher

Wiley

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