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Vascular Immunity and Ischemic Stroke
Ischemic stroke is among the most severe diseases threatening human health, of which atherosclerosis is the main pathophysiological basis. In recent years, both basic and clinical studies have confirmed that the immune system plays a core regulatory role in the occurrence and development of atherosclerosis. Some patients with systemic immune diseases are more likely to develop atherosclerosis, and its severity is higher than in patients without systemic immune disorders. Immune cells are also involved in brain tissue damage and repair after ischemic stroke. The clinical application of monoclonal antibodies targeting B cell surface molecules (such as CD20) and survival factors (such as BAFF) in some chronic inflammatory diseases such as rheumatoid arthritis and psoriasis also provides new directions for the immunotherapy in ischemic stroke. However, finding the best target for drug intervention remains the biggest challenge and an attractive target for new strategies for ischemic stroke.
Crosstalk between Peripheral and Local Immune Response in the Pathophysiology of Stroke and Neurodegeneration Diseases, Volume II
Accumulating evidence reveals both local and peripheral immune systems participated in the pathophysiology changes of acute and chronic neurological diseases. Immune cell activation facilitates inflammatory response in neurological diseases such as stroke, Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis. The immune response initiated by brain local cells (microglia and astrocytes) and peripheral blood cells (monocytes/macrophages, neutrophil, T cells, B cells), are now commonly thought to contribute “double-edged sword” effects to the progression of neurological diseases, which not only promoting repair and recovery, but also accelerating brain injury. Meanwhile, local and peripheral immune responses have complex crosstalk in the development of post-stroke injury and neurodegeneration disease.
