About this Research Topic
Autoimmune diseases of the central nervous system (CNS) are serious chronic illnesses that affect people of all ages. The most common is multiple sclerosis but there are many others which can cause severe disability. Some examples include neuromyelitis optica, anti-myelin oligodendrocyte glycoprotein disease, autoimmune encephalitis, neuropsychiatric lupus (NPSLE) and there are several other rare neurological autoimmune diseases. Even with treatment, most autoimmune diseases progressively worsen the health status of patients, resulting in a diminished quality of life and placing a significant burden on the public health system and the economy.
Immune responses driven by infiltrating self-antigen-specific effector T cells and self-reactive antibodies produced by B cells within the brain or penetrating brain tissue from the circulation due to the compromised blood brain barrier (BBB), damage nervous system components, causing lesions, demyelination, and neuronal damage. This can eventually lead to fatigue, movement disorders, paralysis, vision and speech impairment, cognitive dysfunction, and other medical problems.
Standard therapies include general immunosuppressants and disease-modifying monoclonal antibodies, which are often associated with adverse side effects and leave patients vulnerable to infections and the development of cancer.
CNS tissues are immune privileged and peripheral immune cells, including cells of the adaptive immune system, do not normally invade the brain due to the regulatory function of BBB. However, in states of neuroinflammation, altered BBB function leads to the increase of the immune cell diversity in the brain and potentially to the transfer of brain-reactive antibodies from the circulation . Advances in single-cell profiling provide deep insights into intricate networks of interactions between infiltrating immune cells, neurons, astrocytes, and microglia. Macrophages, monocytes, dendritic cells, NK cells, B cells, and T cells, including immune cells with regulatory functions (such as myeloid-derived suppressor cells, regulatory T cells, and regulatory B cells) have all been found in the inflamed CNS.
Understanding the contribution of different immune cells to the pathogenesis and regulation of autoimmune responses is critical for evaluating existing therapeutic protocols, searching for new targets, and developing novel therapeutics. The ideal treatment would regulate levels of proinflammatory cytokines and infiltration of autoreactive lymphocytes, as well as restore immune homeostasis and tolerance to relevant autoantigens without affecting systemic immune responses. Novel approaches, particularly adoptive cell-based immunotherapies, have received considerable attention over the past decade. Several preclinical studies have shown that myeloid-derived suppressor cells, regulatory T cells, and regulatory B cells can ameliorate the progression of experimental autoimmune encephalitis.
In this Research Topic, we aim to bring together researchers and clinicians from the fields of autoimmunity and neuroimmunology to describe the role of different immune cells in the progression of autoimmune diseases affecting the CNS in patients or animal models. We welcome the submission of Original Research, Clinical Trial, Case Report, Review, Mini-review and Perspective articles related to, but not limited to, the following subtopics:
(1) Analysis of different immune populations of patients (blood, cerebrospinal fluid, brain tissue) suffering from autoimmune CNS diseases
(2) Effect and/or comparison of different therapies (general immunosuppressants, disease-modifying monoclonal antibodies) on immune populations in the CNS
(3) Dynamics of regulatory T cells (Treg), regulatory B cells (Breg) and myeloid-derived suppressor cells (MDSC) during autoimmune disease progression and/or treatment protocols
(4) Cell-based immunotherapies with regulatory immune cells (Treg, Breg, MDSC, tolerogenic dendritic cells, etc.)
Keywords: CNS autoimmune disorders, immunotherapy, neuroinflammation, CNS resident and infiltrating immune cells
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