16/6-idiotype expressing antibodies induce brain inflammation and cognitive impairment in mice: the mosaic of central nervous system involvement in lupus

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dc.creatorShaye, Kivity
dc.creatorKatzav, Aviva
dc.creatorArango, María-Teresa
dc.creatorLandau-Rabi, Moran
dc.creatorZafrir, Yaron
dc.creatorAgmon-Levin, Nancy
dc.creatorBlank, Miri
dc.creatorAnaya, Juan-Manuel
dc.creatorMozes, Edna
dc.creatorChapman, Joab
dc.creatorShoenfeld, Yehuda
dc.date2013-04-04
dc.date2014-08-13T16:32:59Z
dc.date.accessioned2023-11-21T16:12:30Z
dc.date.available2023-11-21T16:12:30Z
dc.descriptionBackground: The 16/6-idiotype (16/6-Id) of the human anti-DNA antibody was found to induce experimental lupus in naive mice, manifested by production of autoantibodies, leukopenia and elevated inflammatory markers, as well as kidney and brain involvement. We assessed behavior and brain pathology of naive mice injected intracerebra-ventricularly (ICV) with the 16/6-Id antibody. Methods: C3H female mice were injected ICV to the right hemisphere with the human 16/6-Id antibody or commercial human IgG antibodies (control). The mice were tested for depression by the forced swimming test (FST), locomotor and explorative activity by the staircase test, and cognitive functions were examined by the novel object recognition and Y-maze tests. Brain slices were stained for inflammatory processes. Results: 16/6-Id injected mice were cognitively impaired as shown by significant differences in the preference for a new object in the novel object recognition test compared to controls (P = 0.012). Similarly, the preference for spatial novelty in the Y-maze test was significantly higher in the control group compared to the 16/6-Id-injected mice (42% vs. 9%, respectively, P = 0.065). Depression-like behavior and locomotor activity were not significantly different between the16/6-Id-injected and the control mice. Immunohistochemistry analysis revealed an increase in astrocytes and microglial activation in the hippocampus and amygdala, in the 16/6-Id injected group compared to the control. Conclusions: Passive transfer of 16/6-Id antibodies directly into mice brain resulted in cognitive impairments and histological evidence for brain inflammation. These findings shed additional light on the diverse mosaic pathophysiology of neuropsychiatric lupus.
dc.formatRecurso electrónico
dc.formatapplication/pdf
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dc.identifierISSN:1741-7015
dc.identifierhttp://repository.urosario.edu.co/handle/10336/8833
dc.identifier.urihttp://repository-salesiana.heoq.net/handle/123456789/272834
dc.languageeng
dc.publisherUniversidad del Rosario
dc.relationhttp://www.biomedcentral.com/1741-7015/11/90
dc.rightsinfo:eu-repo/semantics/openAccess
dc.sourceinstname:Universidad del Rosario
dc.sourcereponame:Repositorio Institucional EdocUR
dc.subjectEnfermedades
dc.subjectAnticuerpos
dc.subjectLupus eritematoso sistémico
dc.subjectEnfermedades autoinmunes
dc.subjectMONOCLONAL ANTI-DNA
dc.subjectTISSUE-BOUND IMMUNOGLOBULINS
dc.subjectHUMAN-HUMAN HYBRIDOMAS
dc.subjectP-PROTEINS PENETRATE
dc.subjectANTIPHOSPHOLIPID SYNDROME
dc.subjectNEUROPSYCHIATRIC LUPUS
dc.subjectTOLEROGENIC PEPTIDE
dc.subjectRECOGNITION MEMORY
dc.subjectSLE PATIENTS
dc.subjectAUTOANTIBODIES
dc.title16/6-idiotype expressing antibodies induce brain inflammation and cognitive impairment in mice: the mosaic of central nervous system involvement in lupus
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/acceptedVersion
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