The balance between the immune system and its metabolism is becoming an effective therapeutic alternative in various inflammatory diseases, including organ transplantation. The interaction between the immune and metabolic pathways play a critical role in dictating disease pathology and progression, and the differences in the bioenergetic demands between immune cells enable them to differentiate into effector and regulatory cells. Recent studies have suggested that changes in intracellular metabolic programs control T cell activation, proliferation and differentiation into T effector (Teffs) or T regulatory cells (Tregs), and metabolic differences between Tregs and Teffs can shift the balance toward a more specific immune tolerance in organ rejection. Pharmacological targeting of T cells metabolism affects the balance between effector and regulatory function of T cells.This therapeutic modulation are of great interest in cancer, autoimmunity, and organ transplantation. In this review, we discuss major metabolic pathways that influence the activation, proliferation and differentiation of Tregs, and also special emphasis on liver kinase B1 (LKB1) pathway that provide stability of Tregs. We also highlight how Tregs metabolic regulome and LKB1 signaling pathway relationship contribute to rescue organ transplants from associated injuries and chronic rejection.
Asthma is a chronic inflammatory disease of the airways, which is considered to be mediated by the allergen-specific CD4+ T cells, Th2 cytokines, and allergen-specific IgE antibodies to play a key role in the initiation and perpetuation of chronic airway inflammation. The most common clinical manifestations of asthma are characterized by airway inflammation, airway obstruction, airway hyperresponsiveness, and airway microvascular remodeling. In addition to inflammatory cells, a tiny population of T regulatory cells (Tregs) control immune homeostasis, suppress allergic responses and participate in the resolution of inflammation-associated tissue injuries. Preclinical studies from animal models have demonstrated the huge therapeutic potential of Tregs in asthma conditions. Increasing evidence indicates that Tregs could be used to inhibit pathogenic asthma inflammation, and airway microvascular remodeling during the progression of asthma. This review addresses the relationship between locally accumulated Tregs and the development of asthmatic inflammation, and associated airway remodeling during the disease progression.