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Your search keyword '"Antel, Jack P."' showing total 45 results
Start Over Author "Antel, Jack P." Journal annals of neurology
45 results on '"Antel, Jack P."'

1. Human Oligodendrocyte Myelination Potential; Relation to Age and Differentiation

Author

Luo, Julia Xiao Xuan, primary, Cui, Qiao‐Ling, additional, Yaqubi, Moein, additional, Hall, Jeffery A., additional, Dudley, Roy, additional, Srour, Myriam, additional, Addour, Nassima, additional, Jamann, Hélène, additional, Larochelle, Catherine, additional, Blain, Manon, additional, Healy, Luke M., additional, Stratton, Jo Anne, additional, Sonnen, Joshua A., additional, Kennedy, Timothy E., additional, and Antel, Jack P., additional

Published
2022
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3. Sublethal oligodendrocyte injury: A reversible condition in multiple sclerosis?

Author

Cui, Qiao-Ling, primary, Khan, Damla, additional, Rone, Malena, additional, T.S. Rao, Vijayaraghava, additional, Johnson, Radia Marie, additional, Lin, Yun Hsuan, additional, Bilodeau, Philippe-Antoine, additional, Hall, Jeffery A., additional, Rodriguez, Moses, additional, Kennedy, Timothy E., additional, Ludwin, Samuel K., additional, and Antel, Jack P., additional

Published
2017
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4. Reply

Author

Bennett, Jeffrey L., primary, Owens, Gregory P., additional, Gilden, Don, additional, Antel, Jack P., additional, and Hemmer, Bernard, additional

Published
2010
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5. Intrathecal pathogenic anti–aquaporin-4 antibodies in early neuromyelitis optica

Author

Bennett, Jeffrey L., primary, Lam, Chiwah, additional, Kalluri, Sudhakar Reddy, additional, Saikali, Philippe, additional, Bautista, Katherine, additional, Dupree, Cecily, additional, Glogowska, Magdalena, additional, Case, David, additional, Antel, Jack P., additional, Owens, Gregory P., additional, Gilden, Don, additional, Nessler, Stefan, additional, Stadelmann, Christine, additional, and Hemmer, Bernhard, additional

Published
2009
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7. Corrections

Author

Niino, Masaaki, primary, Bodner, Caroline, additional, Simard, Marie‐Lune, additional, Alatab, Sudabeh, additional, Gano, Dawn, additional, Kim, Ho Jin, additional, Trigueiro, Manuela, additional, Racicot, Denise, additional, Guérette, Christine, additional, Antel, Jack P., additional, Fournier, Alyson, additional, Grand'Maison, Francois, additional, and Bar‐Or, Amit, additional

Published
2006
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8. Natalizumab effects on immune cell responses in multiple sclerosis

Author

Niino, Masaaki, primary, Bodner, Caroline, additional, Simard, Marie-Lune, additional, Alatab, Sudabeh, additional, Gano, Dawn, additional, Kim, Ho Jin, additional, Trigueiro, Manuela, additional, Racicot, Denise, additional, Guérette, Christine, additional, Antel, Jack P., additional, Fournier, Alyson, additional, Grand'Maison, Francois, additional, and Bar-Or, Amit, additional

Published
2006
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12. Reply

Author

Antel, Jack P., primary and Prat, Alexandre, additional

Published
2000
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24. Reply

Author

Freedman, Mark S., primary, Ruijs, Theodore C. G., additional, Selin, Liisa K., additional, and Antel, Jack P., additional

Published
1992
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27. Intrathecal pathogenic anti-aquaporin-4 antibodies in early neuromyelitis optica.

Author

Bennett, Jeffrey L., Lam, Chiwah, Kalluri, Sudhakar Reddy, Saikali, Philippe, Bautista, Katherine, Dupree, Cecily, Glogowska, Magdalena, Case, David, Antel, Jack P., Owens, Gregory P., Gilden, Don, Nessler, Stefan, Stadelmann, Christine, and Hemmer, Bernhard

Abstract

Objective The serum of most neuromyelitis optica (NMO) patients contains autoantibodies (NMO-IgGs) directed against the aquaporin-4 (AQP4) water channel located on astrocyte foot processes in the perivessel and subpial areas of the brain. Our objectives were to determine the source of central nervous system (CNS) NMO-IgGs and their role in disease pathogenesis. Methods Fluorescence-activated cell sorting and single-cell reverse transcriptase polymerase chain reaction were used to identify overrepresented plasma cell immunoglobulin (Ig) sequences in the cerebrospinal fluid (CSF) of an NMO patient after a first clinical attack. Monoclonal recombinant antibodies (rAbs) were generated from the paired heavy and light chain sequences and tested for target specificity and Fc effector function. The effect of CSF rAbs on CNS immunopathology was investigated by delivering single rAbs to rats with experimental autoimmune encephalomyelitis (EAE). Results Repertoire analysis revealed a dynamic, clonally expanded plasma cell population with features of an antigen-targeted response. Using multiple independent assays, 6 of 11 rAbs generated from CSF plasma cell clones specifically bound to AQP4. AQP4-specific rAbs recognized conformational epitopes and mediated both AQP4-directed antibody-dependent cellular cytotoxicity and complement-mediated lysis. When administered to rats with EAE, an AQP4-specific NMO CSF rAb induced NMO immunopathology: perivascular astrocyte depletion, myelinolysis, and complement and Ig deposition. Interpretation Molecular characterization of the CSF plasma cell repertoire in an early NMO patient demonstrates that AQP4-specfic Ig is synthesized intrathecally at disease onset and directly contributes to CNS pathology. AQP4 is now the first confirmed antigenic target in human demyelinating disease. Ann Neurol 2009;66:617-629 [ABSTRACT FROM AUTHOR]

Published
2009
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28. Substantial early, but nonprogressive neuronal loss in multiple sclerosis (ms) spinal cord.

Author

Schirmer, Lucas, Albert, Monika, Buss, Armin, Schulz-Schaeffer, Walter J., Antel, Jack P., Brück, Wolfgang, and Stadelmann, Christine

Abstract

Research in multiple sclerosis (MS) has recently been focusing on the extent of neuroaxonal damage and its contribution to disease outcome. In the present study, we examined spinal cord tissue from 30 clinically well-characterized MS patients. MS, amyotrophic lateral sclerosis (ALS), and control spinal cord tissue were subjected to morphometric analysis and immunohistochemistry for markers of cell damage and regeneration. Data were related to disease duration and age at death. Here, we present evidence for substantial, nonprogressive neuronal loss on the cervical and lumbar levels early in the disease course of MS. Chromatolytic neurons and immunoreactivity for c-Jun and GAP43 were observed in the ventral gray matter in and adjacent to actively demyelinating lesions, pointing toward neuronal damage and regeneration as an early response to lesion formation. Ann Neurol 2009;66:698-704 [ABSTRACT FROM AUTHOR]

Published
2009
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41. NBI-5788, an altered MBP83-99 peptide, induces a T-helper 2–like immune response in multiple sclerosis patients

Author

Crowe, Paul D., Qin, Yufen, Conlon, Paul J., and Antel, Jack P.

Abstract

We assessed the immune response induced in multiple sclerosis (MS) patients who had received NBI-5788, an altered peptide ligand (APL) designed from an immunodominant region (83–99) of the neuroantigen myelin basic protein (MBP) (5, 10, or 20 mg subcutaneously weekly for 4 weeks). The mean frequency of NBI-5788–responsive T cells (stimulation index > 3) in MS patients treated with the APL was 35.8 ± 12.8% (n = 7) compared with a mean frequency of 6.2 ± 1.3% (n = 7) for the untreated patients. The mean frequency of whole MBP–responsive T cells in MS patients treated with the APL was not significantly different from that of untreated patients (16.4 ± 5.7% vs 18.0 ± 6.3%, respectively). NBI-5788–reactive T-cell lines generated from NBI-5788–treated patients exhibited an increased frequency of cross-reactivity with MBP peptide 83–99 compared with NBI-5788–reactive lines from control MS patients. Cytokine secretion by APL-reactive T-cell lines from NBI-5788–treated MS patients was more frequently T-helper 2–like compared with T-cell lines from untreated MS patients. These results demonstrate that subcutaneous administration of a soluble APL based on the MBP peptide 83–99 in MS patients can induce an APL-reactive immune response in which T lymphocytes cross-reactive with the immunodominant neuroantigen MBP secrete anti-inflammatory cytokines. The significant heterogeneity in immune response between individuals indicates the need for clinical laboratory correlation during the course of therapeutic trials. Ann Neurol 2000;48:758–765

Published
2000
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42. Migratory behavior of lymphocytes isolated from multiple sclerosis patients: Effects of interferon β‐1b therapy

Author

Uhm, Joon H., Dooley, Nora P., Stuve, Olaf, Francis, Gordon S., Duquette, Pierre, Antel, Jack P., and Yong, Voon Wee

Abstract

Previous reports by our group and by others have shown that in vitro treatment of T cells derived from healthy, normal subjects with interferon β‐1b (IFN‐β1b) reduces metalloproteinase (metalloproteinase type 9 [MMP‐9]) activity with a consequent reduction in lymphocyte migration. In this study, we used a Boyden chamber assay to assess the migratory capacity of T cells derived from multiple sclerosis patients who either did or did not receive IFN‐β1b. Lymphocytes derived from patients treated for less than 2 years with IFN‐β migrated at a low rate that was indistinguishable from that of cells isolated from healthy donors. However, longer term treatment with IFN (>3.5 years) was associated with a reversion of the migration to a high level that did not differ statistically from that of cells isolated from untreated multiple sclerosis patients. For both high‐migratory groups, migration could be reduced to control levels after the exogenous addition of TIMP‐1, a relatively specific inhibitor of the MMP‐9, implicating this protease in the process of T‐cell migration. Our findings suggest that one of the mechanisms by which IFN‐β exerts its action is by reducing MMP‐9 activity and thus the entry of inflammatory cells into the nervous system and, as such, MMPs may constitute potential therapeutic targets in inflammatory diseases such as multiple sclerosis.

Published
1999
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43. Recommendations from the national multiple sclerosis society clinical outcomes assessment task force

Author

Rudick, Richard, Antel, Jack, Confavreux, Christian, Cutter, Gary, Ellison, George, Fischer, Jill, Lublin, Fred, Miller, Aaron, Petkau, John, Rao, Stephen, Reingold, Stephen, Syndulko, Karl, Thompson, Alan, Wallenberg, Joy, Weinshenker, Brian, and Willoughby, Ernest

Abstract

This article provides recommendations from the National Multiple Sclerosis Society's Clinical Outcomes Assessment Task Force. The Task Force was appointed in 1994 and charged with recommendending improved approaches for clinical outcomes assessment in future controlled clinical trials. The recommendations herein follow extensive deliberation and data analysis during 2.5 years. General principles and desirable measurement attributes were used to assess alternative measurement techniques and clinical scales. On the basis of the analysis of existing multiple sclerosis (MS) data sets, a new measurement approach is proposed. The approach is based on quantitative functional composites that consist of simple quantitative measures from the major clinical dimensions of MS combined into a single score. Quantitative functional composites are likely to provide improved precision and sensitivity in future MS clinical trials. Studies necessary to further refine quantitative functional composites as useful MS clinical trial outcomes are delineated.

Published
1997
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44. In vivo differentiation of astrocytic brain tumors and isolated demyelinating lesions of the type seen in multiple sclerosis using 1H magnetic resonance spectroscopic imaging

Author

De Stefano, Nicola, Caramanos, Zografos, Preul, Mark C., Francis, Gordon, Antel, Jack P., and Arnold, Douglas L.

Abstract

We used computer pattern recognition of proton magnetic resonance spectroscopic image data to differentiate between brain tumors and large, isolated, demyelinating lesions of the type seen in multiple sclerosis. Leave‐one‐out linear discriminant analyses correctly classified resonance profiles from five acute demyelinating lesions, 20 low‐grade astrocytomas, 22 anoplastic astrocytomas, and 24 glioblastomas. Classification of nonacute lesions will require further development, as the metabolic profiles of demyelinating lesions evolve over time.

Published
1998
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