IgA autoantibodies in Alzheimer Disease✨✨
Welcome back after hopefully a nice enjoyable summer break. Before the holidays JJP Biologics published a series of posts highlighting published scientific papers about the role of the CD89-IgA axis in a subgroup of RA patients which are non-responsive to current therapies, have high IgA autoantibody levels and consequently more severe disease and pathology.
Although, Alzheimer Disease (AD) is no recognised as autoimmune nor as a fibrotic disease, accumulating evidence exists to shows clear evidence of involvement of the peripheral immune system. The presence of chronic neuroinflammation, breaches in the blood-brain barrier (BBB), and increased levels of inflammatory mediators are central to the pathogenesis of AD. These factors promote the penetration of immune cells into the brain, potentially exacerbating clinical symptoms and neuronal death in AD patients. While microglia, the resident immune cells of the central nervous system, play a crucial role in AD, recent evidence suggests the infiltration of cerebral vessels and parenchyma by peripheral immune cells, including neutrophils, T lymphocytes, B lymphocytes, NK cells, and monocytes in AD.
https://lnkd.in/dGy528ZF
Obviously, if peripheral immune cells can use the breaches in the BBB, autoantibodies are also able to penetrate the CNS into the lesions. More evidence of the involvement of IgA antibodies will be the subject of the next few weeks of JJP Biologics scientific posts.
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