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2012 ; 248
(1
): 56-67
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A model for lupus brain disease
#MMPMID22725954
Diamond B
; Volpe BT
Immunol Rev
2012[Jul]; 248
(1
): 56-67
PMID22725954
show ga
Systemic lupus erythematosus is an autoimmune disease characterized by antibodies
that bind target autoantigens in multiple organs in the body. In peripheral
organs, immune complexes engage the complement cascade, recruiting blood-borne
inflammatory cells and initiating tissue inflammation. Immune complex-mediated
activation of Fc receptors on infiltrating blood-borne cells and tissue resident
cells amplifies an inflammatory cascade with resulting damage to tissue function,
ultimately leading to tissue destruction. This pathophysiology appears to explain
tissue injury throughout the body, except in the central nervous system. This
review addresses a paradigm we have developed for autoantibody-mediated brain
damage. This paradigm suggests that antibody-mediated brain disease does not
depend on immune complex formation but rather on antibody-mediated alterations in
neuronal activation and survival. Moreover, antibodies only access brain tissue
when blood-brain barrier integrity is impaired, leading to a lack of concurrence
of brain disease and tissue injury in other organs. We discuss the implications
of this model for lupus and for identifying other antibodies that may contribute
to brain disease.
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