The activation, differentiation, and proliferation of immune cells are supported by their unique metabolic programming. Indeed, the extracellular metabolic microenvironment, including the concentration of glucose, lipids, and amino acids, can also affect the metabolic program of immune cells and their offspring, to determine the phenotype of immune cells and intervene the direction of the immune response. Accordingly, abnormal metabolism programming always contributes to the abnormal processes of immune cells, such as the aberrant autoantigen uptake, presentation of DC or macrophage, activation of T cells and B cells, functional impairments of T or B regulatory cells (Tregs/Bregs), which plays critical roles in the progress of autoimmune diseases, like T1D, SLE, RA, etc.
According to the above concept, we believe it will provide valuable clues for blocking, delaying, and even curing autoimmune diseases when we clarify the metabolic mechanisms of these abnormal immune activities. The discovery during this process will expand our understanding of autoimmunity. Furthermore, the finding of agonists and inhibitors targeting these molecules can become effective therapeutic and research drugs.
Here we welcome you to submit the Original Research, Review, Mini-Review, Hypothesis Theory, and Perspective articles that cover, but are not limited to the sub-topics:
1. Metabolic programming of abnormally activated/ functional impairment immune cells in the process of autoimmune progression.
2. The clarification of specific metabolites which initiate or promote the activation, proliferation, and differentiation of immune cells in the autoimmune targeted tissues/organs.
3. The effects and mechanisms of inhibitors/ agonists of glucose, lipid, and amino acid metabolic pathways on immune responses of autoimmune disease.
The activation, differentiation, and proliferation of immune cells are supported by their unique metabolic programming. Indeed, the extracellular metabolic microenvironment, including the concentration of glucose, lipids, and amino acids, can also affect the metabolic program of immune cells and their offspring, to determine the phenotype of immune cells and intervene the direction of the immune response. Accordingly, abnormal metabolism programming always contributes to the abnormal processes of immune cells, such as the aberrant autoantigen uptake, presentation of DC or macrophage, activation of T cells and B cells, functional impairments of T or B regulatory cells (Tregs/Bregs), which plays critical roles in the progress of autoimmune diseases, like T1D, SLE, RA, etc.
According to the above concept, we believe it will provide valuable clues for blocking, delaying, and even curing autoimmune diseases when we clarify the metabolic mechanisms of these abnormal immune activities. The discovery during this process will expand our understanding of autoimmunity. Furthermore, the finding of agonists and inhibitors targeting these molecules can become effective therapeutic and research drugs.
Here we welcome you to submit the Original Research, Review, Mini-Review, Hypothesis Theory, and Perspective articles that cover, but are not limited to the sub-topics:
1. Metabolic programming of abnormally activated/ functional impairment immune cells in the process of autoimmune progression.
2. The clarification of specific metabolites which initiate or promote the activation, proliferation, and differentiation of immune cells in the autoimmune targeted tissues/organs.
3. The effects and mechanisms of inhibitors/ agonists of glucose, lipid, and amino acid metabolic pathways on immune responses of autoimmune disease.