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.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117 Am+J+Physiol+Renal+Physiol
2016 ; 311
(3
): F487-95
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Optimizing the translational value of animal models of glomerulonephritis:
insights from recent murine prototypes
#MMPMID27335377
Foster MH
Am J Physiol Renal Physiol
2016[Sep]; 311
(3
): F487-95
PMID27335377
show ga
Animal models are indispensable for the study of glomerulonephritis, a group of
diseases that destroy kidneys but for which specific therapies do not yet exist.
Novel interventions are urgently needed, but their rational design requires
suitable in vivo platforms to identify and test new candidates. Animal models can
recreate the complex immunologic microenvironments that foster human autoimmunity
and nephritis and provide access to tissue compartments not readily examined in
patients. Study of rat Heymann nephritis identified fundamental disease
mechanisms that ultimately revolutionized our understanding of human membranous
nephropathy. Significant species differences in expression of a major target
antigen, however, and lack of spontaneous autoimmunity in animals remain
roadblocks to full exploitation of preclinical models in this disease. For
several glomerulonephritides, humanized models have been developed to circumvent
cross-species barriers and to study the effects of human genetic risk variants.
Herein we review humanized mouse prototypes that provide fresh insight into
mediators of IgA nephropathy and origins of antiglomerular basement membrane
nephritis and Goodpasture's disease, as well as a means to test novel therapies
for ANCA vasculitis. Additional and refined model systems are needed to mirror
the full spectrum of human disease in a genetically diverse population, to
facilitate development of patient-specific interventions, to determine the origin
of nephritogenic autoimmunity, and to define the role of environmental exposures
in disease initiation and relapse.
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