Antibody deposition in the stria vascularis of the MRL-Fas(lpr) mouse

Citation
Mj. Ruckenstein et L. Hu, Antibody deposition in the stria vascularis of the MRL-Fas(lpr) mouse, HEARING RES, 127(1-2), 1999, pp. 137-142
Citations number
20
Language
INGLESE
art.tipo
Article
Categorie Soggetti
da verificare
Journal title
HEARING RESEARCH
ISSN journal
0378-5955 → ACNP
Volume
127
Issue
1-2
Year of publication
1999
Pages
137 - 142
Database
ISI
SICI code
0378-5955(199901)127:1-2<137:ADITSV>2.0.ZU;2-Z
Abstract
The MRL-Fas(lpr) mouse, a model of multisystemic, organ non-specific autoim mune disease, has been proposed as a model of immune-mediated inner ear dis ease. Preliminary studies indicate that it develops cochlear pathology focu sed in the stria vascularis including intracellular edema and degeneration which develops in the absence of an inflammatory infiltrate but in the pres ence of antibody deposition. It was thus hypothesized that the antibodies f ound in the stria were mediating a direct pathologic effect on this structu re, without recruiting classical inflammatory mediators. It was further hyp othesized that the antibodies deposited within the stria would be derived f rom the non-complement fixing isotypes and subclasses, which are known to b e able to mediate direct pathologic effects on target tissues. This study u tilized immunohistologic techniques to identify the antibody isotypes and s ubclasses deposited within the stria vascularis of the MRL-Fas(lpr) mouse. Results indicate that all antibody isotypes and subclasses can be identifie d within the stria vascularis in the absence of complement. Thus, antibody deposition was not restricted to non-complement fixing antibodies. While it is possible that antibodies are mediating direct pathologic effects within the stria, the non-specific nature of the antibody deposition may indicate that these antibodies are not responsible for the observed pathology. Rath er, other mechanisms, such as metabolic and genetic etiologies, must also b e considered. (C) 1999 Published by Elsevier Science B.V. All rights reserv ed.