Organisms and potentially harmful environmental stimuli are under a never-ending reciprocal influence. The nervous and immune systems, the interfaces between the internal and the external world, have been traditionally thought as separate entities. In truth they are deeply integrated and complementary, and their cooperation in local and systemic reflexes is crucial for the restoration of homeostasis following tissue injury and infections. The nervous system is continuously monitored by immune cells, which include resident microglia as well as lymphocytes recirculating between the tissue and the cerebrospinal fluid. Although immune cells in the nervous system are present in smaller numbers compared to other organs, our interpretation of the nervous system as an “immune privileged site” has shifted to that of a “special immune-controlled site”, and the importance of immune regulation in the maintenance of homeostasis and in the prevention of diseases is now very clear.
Multiple mechanisms regulate the magnitude of immune responses to curtail overt inflammation and tissue damage and to restore physiological, steady-state, conditions. Nonetheless, inappropriate and uncontrolled immune responses may still occur, leading to chronic and inflammatory disease. Evidence suggests that many neurological disorders may be linked to the breakdown of immune tolerance. Despite the existence of highly efficient regulatory mechanisms to prevent autoimmunity, some autoreactive B and T lymphocytes targeting self-antigens may escape. In combination with an underlying genetic susceptibility and with enhancing environmental factors, these autoreactive cells may contribute to the development of many neurological disorders and this is strongly supported by animal models and human studies. Crucially, pathogenic immune cells have been reported to have impaired metabolism and in the past few years experimental evidence has revealed that shifts or defects in metabolic programs of immune cells can support the pathogenesis of autoimmune diseases in CNS leading to metabolic pathways emerging as crucial targets to treat autoimmune disease.
In this Research Topic we aim to emphasize the fundamental role of the immune system’s balance as a key element in the crosstalk with the nervous system, with particular focus in the consequences of its dysregulation on the emergence of disease.
We welcome the submissions of Original Research, Brief Research Report, Perspective and Review articles on human and/or animal studies, covering the role of T cell lymphocytes in immune-mediated neurological disorders with particular emphasis on the following topics:
1. Defects of cell-mediated immunity in neurological diseases
2. Role of autoreactive CD4+ and CD8+ T cells targeting self-neuronal antigens as immune cells mediators of disorders of the central and peripheral nervous system
3. Role of cells with immune-regulatory functions in CNS disorders
4. Systemic and intracellular metabolic alterations in central and peripheral nervous system disorders
Organisms and potentially harmful environmental stimuli are under a never-ending reciprocal influence. The nervous and immune systems, the interfaces between the internal and the external world, have been traditionally thought as separate entities. In truth they are deeply integrated and complementary, and their cooperation in local and systemic reflexes is crucial for the restoration of homeostasis following tissue injury and infections. The nervous system is continuously monitored by immune cells, which include resident microglia as well as lymphocytes recirculating between the tissue and the cerebrospinal fluid. Although immune cells in the nervous system are present in smaller numbers compared to other organs, our interpretation of the nervous system as an “immune privileged site” has shifted to that of a “special immune-controlled site”, and the importance of immune regulation in the maintenance of homeostasis and in the prevention of diseases is now very clear.
Multiple mechanisms regulate the magnitude of immune responses to curtail overt inflammation and tissue damage and to restore physiological, steady-state, conditions. Nonetheless, inappropriate and uncontrolled immune responses may still occur, leading to chronic and inflammatory disease. Evidence suggests that many neurological disorders may be linked to the breakdown of immune tolerance. Despite the existence of highly efficient regulatory mechanisms to prevent autoimmunity, some autoreactive B and T lymphocytes targeting self-antigens may escape. In combination with an underlying genetic susceptibility and with enhancing environmental factors, these autoreactive cells may contribute to the development of many neurological disorders and this is strongly supported by animal models and human studies. Crucially, pathogenic immune cells have been reported to have impaired metabolism and in the past few years experimental evidence has revealed that shifts or defects in metabolic programs of immune cells can support the pathogenesis of autoimmune diseases in CNS leading to metabolic pathways emerging as crucial targets to treat autoimmune disease.
In this Research Topic we aim to emphasize the fundamental role of the immune system’s balance as a key element in the crosstalk with the nervous system, with particular focus in the consequences of its dysregulation on the emergence of disease.
We welcome the submissions of Original Research, Brief Research Report, Perspective and Review articles on human and/or animal studies, covering the role of T cell lymphocytes in immune-mediated neurological disorders with particular emphasis on the following topics:
1. Defects of cell-mediated immunity in neurological diseases
2. Role of autoreactive CD4+ and CD8+ T cells targeting self-neuronal antigens as immune cells mediators of disorders of the central and peripheral nervous system
3. Role of cells with immune-regulatory functions in CNS disorders
4. Systemic and intracellular metabolic alterations in central and peripheral nervous system disorders