An imbalance in T cell phenotype switching triggers autoimmune disorders. The imbalance may initiate during the regulation of any of the interconnected cellular components that modulate T cell biology: environmental cues, signaling pathways, cytokine-mediated regulation, cell-to-cell communication, cell cycle, metabolism, and microbiome. Failure of the coordination among these responses may kickstart the process of anomalous Th cell behavior, with the resulting Th cell phenotype imbalance potentially resulting in a switch from a healthy state to a disease state, thereby in the onset of autoimmune/autoinflammatory disorders.
The study of molecular signalling pathways in the fate of immune cells has gained relevance for their potential dysregulation in the onset of diseases of the immune system. Indeed, the signalling and metabolic pathways involved in the proliferation, development, and differentiation of different immune cell types have attracted the interest of the scientific and patient communities. In recent years, new evidence about the involvement of particular cell populations in the development of autoimmune disorders has been shown. An example is given by T cells, which metabolic status we have recently proposed to be the tipping point underlying the imbalance among T cell types in healthy versus immunocompromised patients. 1 Thus, understanding the context of the development of T and B cell subtypes in different tissues, and the cues responsible for their emergence, appears to be crucial when treating autoimmune disorders.Recently, the work of Liu and colleagues presented new data that support the role of the Mst1/Akt/STAT axis in the development of central and peripheral B cell populations in CC chemokine receptor type 2 (CCR2) wildtype and knockout mice. 2 CCR2 is a chemokine receptor that transduces signals in inflammatory diseases and the inflammatory response against cancer, upon binding of the chemokine (C-C motif) ligand 2 (CCL2) that mediates monocyte chemotaxis. Liu and colleagues observe an increased CCR2 expression in the peripheral bloodThis is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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