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BAFF is produced by astrocytes and up-regulated in multiple sclerosis lesions and primary central nervous system lymphoma 总被引:13,自引:0,他引:13 下载免费PDF全文
Krumbholz M Theil D Derfuss T Rosenwald A Schrader F Monoranu CM Kalled SL Hess DM Serafini B Aloisi F Wekerle H Hohlfeld R Meinl E 《The Journal of experimental medicine》2005,201(2):195-200
We report that B cell-activating factor of the tumor necrosis factor (TNF) family (BAFF) is expressed in the normal human brain at approximately 10% of that in lymphatic tissues (tonsils and adenoids) and is produced by astrocytes. BAFF was regularly detected by enzyme-linked immunosorbent assay in brain tissue lysates and in normal spinal fluid, and in astrocytes by double fluorescence microscopy. Cultured human astrocytes secreted functionally active BAFF after stimulation with interferon-gamma and TNF-alpha via a furin-like protease-dependent pathway. BAFF secretion per cell was manifold higher in activated astrocytes than in monocytes and macrophages. We studied brain lesions with B cell components, and found that in multiple sclerosis plaques, BAFF expression was strongly up-regulated to levels observed in lymphatic tissues. BAFF was localized in astrocytes close to BAFF-R-expressing immune cells. BAFF receptors were strongly expressed in situ in primary central nervous system (CNS) lymphomas. This paper identifies astrocytes as a nonimmune source of BAFF. CNS-produced BAFF may support B cell survival in inflammatory diseases and primary B cell lymphoma. 相似文献
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Irina Alafuzoff Dietmar R. Thal Thomas Arzberger Nenad Bogdanovic Safa Al-Sarraj Istvan Bodi Susan Boluda Orso Bugiani Charles Duyckaerts Ellen Gelpi Stephen Gentleman Giorgio Giaccone Manuel Graeber Tibor Hortobagyi Romana Höftberger Paul Ince James W. Ironside Nikolaos Kavantzas Andrew King Penelope Korkolopoulou Gábor G. Kovács David Meyronet Camelia Monoranu Tatjana Nilsson Piero Parchi Efstratios Patsouris Maria Pikkarainen Tamas Revesz Annemieke Rozemuller Danielle Seilhean Walter Schulz-Schaeffer Nathalie Streichenberger Stephen B. Wharton Hans Kretzschmar 《Acta neuropathologica》2009,117(3):309-320
β-Amyloid (Aβ) related pathology shows a range of lesions which differ both qualitatively and quantitatively. Pathologists,
to date, mainly focused on the assessment of both of these aspects but attempts to correlate the findings with clinical phenotypes
are not convincing. It has been recently proposed in the same way as ι and α synuclein related lesions, also Aβ related pathology
may follow a temporal evolution, i.e. distinct phases, characterized by a step-wise involvement of different brain-regions.
Twenty-six independent observers reached an 81% absolute agreement while assessing the phase of Aβ, i.e. phase 1 = deposition
of Aβ exclusively in neocortex, phase 2 = additionally in allocortex, phase 3 = additionally in diencephalon, phase 4 = additionally
in brainstem, and phase 5 = additionally in cerebellum. These high agreement rates were reached when at least six brain regions
were evaluated. Likewise, a high agreement (93%) was reached while assessing the absence/presence of cerebral amyloid angiopathy
(CAA) and the type of CAA (74%) while examining the six brain regions. Of note, most of observers failed to detect capillary
CAA when it was only mild and focal and thus instead of type 1, type 2 CAA was diagnosed. In conclusion, a reliable assessment
of Aβ phase and presence/absence of CAA was achieved by a total of 26 observers who examined a standardized set of blocks
taken from only six anatomical regions, applying commercially available reagents and by assessing them as instructed. Thus,
one may consider rating of Aβ-phases as a diagnostic tool while analyzing subjects with suspected Alzheimer’s disease (AD).
Because most of these blocks are currently routinely sampled by the majority of laboratories, assessment of the Aβ phase in
AD is feasible even in large scale retrospective studies. 相似文献
3.
Staging/typing of Lewy body related α-synuclein pathology: a study of the BrainNet Europe Consortium
Irina Alafuzoff Paul G. Ince Thomas Arzberger Safa Al-Sarraj Jeanne Bell Istvan Bodi Nenad Bogdanovic Orso Bugiani Isidro Ferrer Ellen Gelpi Stephen Gentleman Giorgio Giaccone James W. Ironside Nikolaos Kavantzas Andrew King Penelope Korkolopoulou Gábor G. Kovács David Meyronet Camelia Monoranu Piero Parchi Laura Parkkinen Efstratios Patsouris Wolfgang Roggendorf Annemieke Rozemuller Christine Stadelmann-Nessler Nathalie Streichenberger Dietmar R. Thal Hans Kretzschmar 《Acta neuropathologica》2009,117(6):635-652
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Irina Alafuzoff Maria Pikkarainen Manuela Neumann Thomas Arzberger Safa Al-Sarraj Istvan Bodi Nenad Bogdanovic Orso Bugiani Isidro Ferrer Ellen Gelpi Stephen Gentleman Giorgio Giaccone Manuel B. Graeber Tibor Hortobagyi Paul G. Ince James W. Ironside Nikolaos Kavantzas Andrew King Penelope Korkolopoulou Gábor G. Kovács David Meyronet Camelia Monoranu Tatjana Nilsson Piero Parchi Efstratios Patsouris Tamas Revesz Wolfgang Roggendorf Annemieke Rozemuller Danielle Seilhean Nathalie Streichenberger Dietmar R. Thal Stephen B. Wharton Hans Kretzschmar 《Journal of neural transmission (Vienna, Austria : 1996)》2015,122(7):957-972
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Monoranu CM Huang B Zangen IL Rutkowski S Vince GH Gerber NU Puppe B Roggendorf W 《Cancer Genetics and Cytogenetics》2008,182(1):18-26
Losses and rearrangements of genetic material on chromosome 6q are frequently found in several human malignancies, including primary central nervous system tumors. We previously used microsatellite analysis of ependymomas to identify frequent deletions in regions 6q15 approximately q16, 6q21 approximately q22.1, and 6q24.3 approximately q25.3. To refine our preliminary analysis of potential prognostic regions, we used a panel of 25 microsatellite markers located between 6q15 and 6qter in 49 pairs of matched normal and tumor specimens from 28 children and 21 adults with ependymoma. Allelic deletions were detected in 34 of 49 patients (69%), and two common regions of deletions (6q24.3 and 6q25.2 approximately q25.3) were identified. A short segment of approximately 0.4 Mb between D6S1612 and D6S363 on 6q25.3, containing the SNX9 and SYNJ2 genes, exhibited the highest number of aberrations (n = 38). Pediatric tumors showed slightly fewer aberrations (64%) than adult tumors (76%) and also predominantly exhibited small interstitial deletions, in contrast to the extensive losses of genetic material in adults. Pediatric anaplastic intracranial (supra- and infratentorial) ependymomas harboring the 6q25.3 deletion (n = 9) showed significantly longer overall survival than did patients of the same group without the aberration (n = 6), independent of the extent of resection (P = 0.013). This supports the identified deletion on 6q25.3 as a candidate favorable prognostic parameter and warrants further investigation. 相似文献
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Irina Alafuzoff Maria Pikkarainen Manuela Neumann Thomas Arzberger Safa Al-Sarraj Istvan Bodi Nenad Bogdanovic Orso Bugiani Isidro Ferrer Ellen Gelpi Stephen Gentleman Giorgio Giaccone Manuel B. Graeber Tibor Hortobagyi Paul G. Ince James W. Ironside Nikolaos Kavantzas Andrew King Penelope Korkolopoulou Gábor G. Kovács David Meyronet Camelia Monoranu Tatjana Nilsson Piero Parchi Efstratios Patsouris Tamas Revesz Wolfgang Roggendorf Annemieke Rozemuller Danielle Seilhean Nathalie Streichenberger Dietmar R. Thal Stephen B. Wharton Hans Kretzschmar 《Journal of neural transmission (Vienna, Austria : 1996)》2015,122(7):973-974
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Lukashova-v Zangen I Kneitz S Monoranu CM Rutkowski S Hinkes B Vince GH Huang B Roggendorf W 《Acta neuropathologica》2007,113(3):325-337
Ependymomas are primary tumors of the central nervous system that typically originate from the walls of the cerebral ventricles
or from the spinal canal. The pathogenesis of these tumors is poorly understood, and prognostic assessment based on histologic
features and clinical parameters is difficult. The aim of this study was to investigate the molecular heterogeneity of ependymomas.
We used cDNA microarrays and RT-PCR to examine gene expression in 47 ependymomas. We present results for five comparisons:
(1) tumors from children and adults with poor versus favorable outcome, (2) tumors from children with poor versus favorable
outcome, (3) tumors with high versus low proliferation indices, (4) subependymomas versus myxopapillary ependymomas, and (5)
spinal versus intracranial ependymomas. For patients with an overall survival >10 years after diagnosis, we identified 27
genes associated with favorable prognosis. In contrast, overexpression of BNIP3, MRC1, EPHB3, GLIS3, CDK4, COL4A2, EBP, NRCAM,
and CCNA1 genes in tumors with high proliferation indices was associated with a poor outcome. Thirty genes, including ETV6,
YWHAE, TOP2A, TLR2, IRAK1, TIA1, and UFD1L were found to be highly expressed in subependymomas but not myxopapillary ependymomas.
Also, 30 genes were differentially expressed in spinal versus intracranial ependymomas. There was no relationship between
expression profiles and tumor grade, patient age, and patient gender. Our results provide insight into specific molecular
events underlying ependymoma tumorigenesis and may contribute to more accurate diagnosis and prediction of clinical outcome.
Electronic supplementary material The online version of this article (doi:) contains supplementary material, which is available to authorized users. 相似文献
10.
Comparison analysis of gene expression patterns between sporadic Alzheimer's and Parkinson's disease
Grünblatt E Zander N Bartl J Jie L Monoranu CM Arzberger T Ravid R Roggendorf W Gerlach M Riederer P 《Journal of Alzheimer's disease : JAD》2007,12(4):291-311
Sporadic Alzheimer's (AD) and Parkinson's disease (PD) are late-onset neurodegenerative diseases with tremendous impact on lives of affected individuals. There is a great probability of developing concurrent Parkinsonism in AD and vice-versa than would be predicted by independent prevalence of each disease. We hypothesize that in sporadic AD as well as PD a combination of environmental effects and gene expression may affect specific brain areas leading to neurodegeneration. We profiled gene expression of AD compared to PD and age matched controls post-mortem in the hippocampus, the gyrus-frontalis-medius (Gfm) and the cerebellum using Gene-Chip microarray (Affymetrix) and quantitative-real-time-RT-PCR. Twelve genes altered in similar manner in AD and PD, while four genes showed differential expression profiles between AD and PD in different brain regions (cannabinoid-receptor-2, Histone-cluster-1-H3e, nicotinic-cholinergic-receptor-alpha6 and beta-site-APP-cleaving enzyme-1). Knowledge of selective gene expression profile can lead to better understanding of disease pathology and development of specific diagnosis and effective therapy. 相似文献