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Autoantibodies to Synaptic Receptors and Neuronal Cell Surface Proteins in
Autoimmune Diseases of the Central Nervous System
#MMPMID28298428
Dalmau J
; Geis C
; Graus F
Physiol Rev
2017[Apr]; 97
(2
): 839-887
PMID28298428
show ga
Investigations in the last 10 years have revealed a new category of neurological
diseases mediated by antibodies against cell surface and synaptic proteins. There
are currently 16 such diseases all characterized by autoantibodies against
neuronal proteins involved in synaptic signaling and plasticity. In clinical
practice these findings have changed the diagnostic and treatment approach to
potentially lethal, but now treatable, neurological and psychiatric syndromes
previously considered idiopathic or not even suspected to be immune-mediated.
Studies show that patients' antibodies can impair the surface dynamics of the
target receptors eliminating them from synapses (e.g., NMDA receptor), block the
function of the antigens without changing their synaptic density (e.g., GABAb
receptor), interfere with synaptic protein-protein interactions (LGI1, Caspr2),
alter synapse formation (e.g., neurexin-3?), or by unclear mechanisms associate
to a new form of tauopathy (IgLON5). Here we first trace the process of discovery
of these diseases, describing the triggers and symptoms related to each
autoantigen, and then review in detail the structural and functional alterations
caused by the autoantibodies with special emphasis in those (NMDA receptor,
amphiphysin) that have been modeled in animals.
|Autoantibodies/*immunology
[MESH]
|Autoimmune Diseases/*immunology
[MESH]
|Central Nervous System Diseases/*immunology
[MESH]
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