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1. P486 Treatment-emergent COVID-19 infections in ozanimod ulcerative colitis and multiple sclerosis clinical trials

Author

Ungaro, R, primary, Siegel, C A, additional, Cree, B A C, additional, Selmaj, K W, additional, Ahmad, H A, additional, Pai, A, additional, Ather, S, additional, Henry, A, additional, Charles, L, additional, Petersen, A, additional, Cheng, C Y, additional, Afsari, S, additional, Sheffield, J, additional, Vaile, J, additional, and Colombel, J F, additional

Published
2022
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7. Alemtuzumab more effective than interferon -1a at 5-year follow-up of CAMMS223 Clinical Trial

Author

Coles, A. J., primary, Fox, E., additional, Vladic, A., additional, Gazda, S. K., additional, Brinar, V., additional, Selmaj, K. W., additional, Skoromets, A., additional, Stolyarov, I., additional, Bass, A., additional, Sullivan, H., additional, Margolin, D. H., additional, Lake, S. L., additional, Moran, S., additional, Palmer, J., additional, Smith, M. S., additional, and Compston, D. A. S., additional

Published
2012
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8. Multiple Sclerosis Severity Score: Using disability and disease duration to rate disease severity

Author

Roxburgh, R. H.S.R., primary, Seaman, S. R., additional, Masterman, T., additional, Hensiek, A. E., additional, Sawcer, S. J., additional, Vukusic, S., additional, Achiti, I., additional, Confavreux, C., additional, Coustans, M., additional, le Page, E., additional, Edan, G., additional, McDonnell, G. V., additional, Hawkins, S., additional, Trojano, M., additional, Liguori, M., additional, Cocco, E., additional, Marrosu, M. G., additional, Tesser, F., additional, Leone, M. A., additional, Weber, A., additional, Zipp, F., additional, Miterski, B., additional, Epplen, J. T., additional, Oturai, A., additional, Sorensen, P. S., additional, Celius, E. G., additional, Lara, N. T., additional, Montalban, X., additional, Villoslada, P., additional, Silva, A. M., additional, Marta, M., additional, Leite, I., additional, Dubois, B., additional, Rubio, J., additional, Butzkueven, H., additional, Kilpatrick, T., additional, Mycko, M. P., additional, Selmaj, K. W., additional, Rio, M. E., additional, Sa, M., additional, Salemi, G., additional, Savettieri, G., additional, Hillert, J., additional, and Compston, D. A.S., additional

Published
2005
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19. Experimental autoimmune encephalomyelitis: Immunotherapy with anti-tumor necrosis factor antibodies and soluble tumor necrosis factor receptors

Author

Selmaj, K. W., Raine, C. S., Waksman, B. H., Nathan, C., Sporn, M., Tracey, K. J., Wei, H., Mannogue, K. R., Selmaj, K., Farooq, M., Norton, W. T., Cannella, B., Brosnan, C. F., Peter, J. B., Boctor, F. N., Tourtellotte, W. W., Franciotta, D. M., Grimaldi, L. M. E., Martino, G. V., Hauser, S. L., Doolittle, T. H., Lincoln, R., Brown, R. H., Dinarello, C. A., Sharief, M. K., Hentges, R., Beck, J., Rondol, L., Calinol, L., Raines, C. S., Anne Cross, Ruddle, N. H., Bergman, C. M., Mcgrath, M. L., Teuscher, C., Hickey, W. F., Korngold, R., Seckinger, P., Idaaz, S., Dayer, J. -M, Kohno, T., Brewer, M. T., Baker, S. L., Papierz, W., Glabinski, A., Cavender, D. E., Edelbaum, D., Ziff, M., Barten, D. M., Hackett, R. J., Davis, L. S., Lipsky, P. E., Brightman, B. K., and Fan, H.

20. Alemtuzumab provides durable improvements in clinical outcomes in treatment-naive patients with active relapsing-remitting multiple sclerosis over 6 years in the absence of continuous treatment (CARE-MS I)

Author

Coles, A. J., Boyko, A. N., Cohen, J. A., De Seze, J., Fox, E. J., Havrdova, E., Hartung, H. -P., Inshasi, J. S., McCombe, P., Selmaj, K. W., Vermersch, P., Van Wijmeersch, Bart, Margolin, D. H., Thangavelu, K., Rodriguez, C. E., and Montalban, X.

Abstract

Sanofi Genzyme and Bayer HealthCare Pharmaceuticals. AJC: Consulting fees, lecture fees, and institutional grant support (Sanofi Genzyme). ANB: Consulting fees/participated in clinical trials (Bayer, Biogen, Merck Serono, Novartis, Sanofi-Aventis, Sanofi Genzyme, and Teva Pharmaceuticals). JAC: Consulting and/or speaking fees (Genentech, Novartis, Sanofi Genzyme); and compensation for serving as a journal editor, associate editor, or member of an editorial advisory board (Multiple Sclerosis Journal: Experimental, Translational and Clinical). EJF: Consulting and/or speaking fees, and grant/research support (Acorda, Bayer, Biogen, Chugai, Eli Lilly, EMD Serono, Genentech, Novartis, Opexa, Roche, Sanofi, Sanofi Genzyme, and Teva Pharmaceuticals). EH: Honoraria and grant support (Actelion, Biogen, Merck Serono, Novartis, Receptos, Roche, Sanofi Genzyme, and Teva) and is supported by Ministry of Education of Czech Republic. H-PH: Consulting and/or speaking fees (Bayer, Biogen, CSL Behring, Grifols, Merck Serono, Novartis, Roche, and Sanofi Genzyme). PM: Consulting and/or speaking fees (Biogen, Novartis, Sanofi-Aventis, and Teva Pharmaceuticals). KWS: Consulting and/or speaking fees (Biogen, Merck, Novartis, Roche, Sanofi Genzyme, and Synthon). PV: Consulting and/or speaking fees, and research support (Almirall, Bayer, Biogen, GlaxoSmithKline, Merck Serono, Novartis, Sanofi Genzyme, and Teva). BVW: Received research and travel grants, honoraria for MS-expert advice, and speakers fees (Bayer-Schering, Biogen, Merck Serono, Novartis, Roche, Sanofi Genzyme, and Teva). DHM, KT, and CER: Employees of Sanofi Genzyme. XM: Consulting and/or speaking fees (Almirall, Bayer, Biogen, EMD, Genentech, Geneuro, Merck, Neurotec, Novartis, Roche, Sanofi, Sanofi Genzyme, and Teva Pharmaceuticals).

32. Circulating adhesion molecules and inflammatory mediators in demyelination: A review

Author

Hartung, H. -P, Archelos, J. J., Zielasek, J., Gold, R., Koltzenburg, M., Reiners, K. -H, Toyka, K. V., Raine, C. S., Hafler, D. A., Weiner, H. L., Chang, J., Utz, U., Mcfarland, H. F., Thomas, P. K., Hartung, H. P., Pollard, J. D., Harvey, G. K., Taylor, W. A., Hughes, R. A. C., Reiners, K., Schmidt, B., Khalili-Shirazi, A., Brostoff, S. W., Burns, J., Krasner, L. J., Rostami, A., Pleasure, D., Pette, M., Gengaroli, C., Linington, C., Brosnan, C. F., Claudio, R. A., Martiney, J. A., Sobel, R. A., Mitchell, M. E., Fondren, G., Hickey, W. F., Shingu, M., Hashimoto, M., Ezaki, I., Nobunaga, M., Springer, T. A., Bevilacqua, M. P., Nelson, R. M., Hynes, R. O., Picker, J., Gearing, A. J. H., Newman, W., Pigott, R., Dillon, L. P., Hemingway, I. H., Brustein, M., Kraal, G., Mebius, R. E., Watson, S. R., Schleiffenbaum, B., Spertini, O., Tedder, T. F., Leeuwenberg, J. F. M., Smeets, E. F., Neefjes, J. J., Seth, R., Raymond, F. D., Makgoba, M. W., Rothlein, R., Manolfi, E. A., Czaikowski, M., Martin, D. S., Tsukada, N., Miyaagi, K., Matsuda, M., Michels, M., Jander, S., Heidenreich, F., Stoll, G., Sharief, M. K., Noori, M. A., Ciardi, M., Rieckmann, P., Weichselbraun, I., Albrecht, M., Mccarron, R. M., Wang, L., Racke, M. K., Jemison, L. M., Williams, S. K., Lublin, F. D., Kim, K. S., Wass, C. A., Cross, A. S., Opal, S. M., Wilcox, C. E., Ward, A. M., Evans, A., Frohman, E. M., Frohman, T. C., Dustin, M. L., Wong, D., Dorovini-Zis, K., Fabry, Z., Waldschmidt, M. M., Hendrickson, D., Satoh, J., Kim, S. U., Kastrukoff, L. F., Takei, F., Whitaker, J. N., Herman, P. K., Sparacio, S. M., Cannella, B., Cross, A. H., Dopp, J. M., Breneman, S. M., Olschowska, J. A., Lindsey, J. W., Steinman, L., Steffen, B. J., Butcher, E. C., Engelhardt, B., Osborn, L., Hession, C., Tizard, R., Baron, J. L., Madri, J. A., Ruddle, N. H., Kuchroo, V. K., Martin, C. A., Greer, J. M., Tanaka, M., Satom, A., Makino, M., Tabira, T., Yednock, T. A., Cannon, C., Fritz Zimprich, Jung, S., Maurer, M., Willenborg, D. O., Simmons, R. D., Tamatani, T., Miyasaka, M., Seventer, G. A., Shimizu, Y., Damle, N. K., Aruffo, A., Dang, L. H., Michalek, M. T., Dougherty, G. J., Murdock, S., Hogg, N., Landis, R. C., Oka, N., Akiguchi, I., Kawasaki, T., Staunton, D. E., Ockenhouse, C. F., Ellison, M. D., Merchant, R. E., Selmaj, K., Zeman, A., Mclean, B., Thompson, E. J., Powell, M. B., Mitchell, D., Lederman, J., Hershkoviz, R., Mor, F., Gilat, D., Kuroda, Y., Shimamoto, Y., Bergman, C. M., Mcgrath, K. M., Chung, I. Y., Norris, J. G., Benveniste, E. N., Hofmann, F. M., Hinton, D. R., Johnson, K., Merrill, J. E., Strom, S. R., Ellison, G. W., Myers, L. W., Rudick, R. A., Ransohoff, R. M., Hentges, R., Trotter, J. L., Collins, K. G., Veen, R. C., Hauser, S. L., Doolittle, T. H., Lincoln, R., Beck, J., Rondot, P., Catinot, L., Chofflon, M., Juillard, C., Juillard, P., Kitze, B., Tracey, K. J., Cerami, A., Miyagi, K., Yanagisawa, N., Selmaj, K. W., Farooq, M., Norton, W. T., Fierz, W., Endler, B., Reske, K., Sun, D., Schafer, B., Meide, P. H., Strigard, K., Holmdahl, R., Meide, P., Tsai, C. P., Armati, P. J., Billiau, A., Duong, T. T., St Louis, J., Gilbert, J. J., Voorthuis, J. A. C., Uitdehaag, B. M. J., Groot, C. J. A., Steiniger, B., Vass, K., Lassmann, H., Vethna, M., Lampson, L. A., Karpus, W. J., Swanborg, R. H., Renno, T., Lin, J. Y., Piccirillo, C., Olsson, T., Wang, W. -Z, Hojeberg, B., Voskuhl, R. R., Martin, R., Bergman, C., Link, J., Soderstrom, M., Colton, C. A., Gilbert, D. L., Sonderer, B., Wild, P., Wyler, R., Nathan, C. F., Heininger, K., Stevens, A., Lang, R., Schabet, M., Bowern, N. A., Danta, G., Doherty, P. D., Griot, C., Burge, T., Vandervelde, M., Peterhans, E., Chia, L. S., Thompson, J. E., Moscarello, M. A., Konat, G. W., Wiggins, R. C., Offner, H., Richard, A., Kolb, H., Kolb-Bachofen, V., Tausch, M., Simmons, M. L., Murphy, S., Macmickin, J. D., Weidenmann, M. J., Koprowski, H., Zheng, Y. M., Heber-Katz, E., Bo, L., Dawson, T. M., Wesselingh, S., Misko, T. P., Lin, R. F., Ignarro, L. J., Sherman, M. P., Levi-Strauss, M., Mallat, M., Compston, D. A., Morgan, B. P., Campbell, A. K., Scolding, N., Noble, M., Koski, C. L., Oleesky, D., Sanders, M. E., Swoveland, P. T., Robbins, D., Schwenke, C., Bitter-Suermann, D., Griffin, J. W., Li, C. Y., Feasby, T. E., Hahn, A. F., Neilson, M., Scolding, N. J., Sawant-Mane, S., Clark, M. B., Piddlesden, S., Zimprich, F., Shin, N. L., and Carney, D. F.

38. Effect of laquinimod on MRI-monitored disease activity in patients with relapsing-remitting multiple sclerosis: a multicentre, randomised, double-blind, placebo-controlled phase IIb study.

Author

Comi, G., Pulizzi, A., Rovaris, M., Abramsky, O., Arbizu, T., Boiko, A., Gold, R., Havrdova, E., Komoly, S., Selmaj, K. W., Sharrack, B., and Filippi, M.

Subjects
*IMMUNOLOGICAL adjuvants, *MULTIPLE sclerosis treatment, *CLINICAL trials, *CLINICAL drug trials, *MAGNETIC resonance imaging, *CLINICAL medicine research, *THERAPEUTICS
Abstract

The article presents the results of a clinical trial on use of the oral drug laquinimod, an immunomodulatory agent, to treat relapsing-remitting multiple sclerosis (MS). The international selection of patients is described, as is the study design and the evaluation of outcomes using magnetic resonance imaging to detect gladolinium-enhancing (GdE) brain lesions. Patients treated with laquinimod were found to have reductions in brain lesions over 36 weeks, and the drug was well tolerated by most subjects.

Published
2008
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39. Multiple sclerosis: the increased frequency of the ICAM-1 exon 6 gene point mutation genetic type K469.

Author

Mycko MP, Kwinkowski M, Tronczynska E, Szymanska B, and Selmaj KW

Subjects
Base Sequence, Case-Control Studies, Chi-Square Distribution, DNA analysis, Gene Frequency, Genetic Linkage, Genetic Testing, Genotype, Humans, Magnetic Resonance Imaging, Multiple Sclerosis diagnosis, Polymorphism, Genetic, Random Allocation, Reference Values, White People genetics, Intercellular Adhesion Molecule-1 genetics, Multiple Sclerosis genetics, Point Mutation
Abstract

Intracellular adhesion molecule-1 (ICAM-1) plays an important role in the cascade of adhesion events in the homing of inflammatory cells to the central nervous system (CNS) in experimental autoimmune encephalomyelitis (EAE) and in multiple sclerosis (MS). Two single-base ICAM-1 polymorphisms have been described, in exons 4 and 6, changing codons 241 and 469 in the ICAM-1 gene, respectively. Both polymorphisms result in amino acid changes and can potentially lead to different interactions of ICAM-1 with its ligands. To detect ICAM-1 gene polymorphisms in MS, we have developed a highly sensitive and site-specific, two-stage, nested polymerase chain reaction. Genomic DNA was extracted from blood cells of 79 MS patients and 68 control subjects. The results were confirmed by direct dideoxy chain termination sequencing. The frequency of exon 6 allele T was found to be significantly higher in MS patients than in controls (68% vs 49%). Most interesting, the frequency of exon 6 homozygote K469 was significantly higher in MS patients than in controls (53% vs 34%). Higher frequency of the K469 genotype was found to be independent of possible linkage with the previously described MS susceptibility factor, the HLA class II DR2 allele. In the present study, we have shown for the first time the ICAM-1 gene polymorphisms in MS. The results indicate increased frequency of ICAM-1 exon 6 allele T in MS patients, which may contribute to the MS genetics background.

Published
1998
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40. Experimental autoimmune encephalomyelitis: immunotherapy with anti-tumor necrosis factor antibodies and soluble tumor necrosis factor receptors.

Author

Selmaj KW and Raine CS

Subjects
Animals, Antigens, CD immunology, Encephalomyelitis, Autoimmune, Experimental immunology, Encephalomyelitis, Autoimmune, Experimental metabolism, Humans, Mice, Multiple Sclerosis immunology, Multiple Sclerosis metabolism, Receptors, Tumor Necrosis Factor metabolism, Receptors, Tumor Necrosis Factor, Type I, Tumor Necrosis Factor-alpha metabolism, Antibodies, Monoclonal therapeutic use, Encephalomyelitis, Autoimmune, Experimental therapy, Immunotherapy, Adoptive, Multiple Sclerosis therapy, Receptors, Tumor Necrosis Factor immunology, Tumor Necrosis Factor-alpha immunology
Abstract

Multiple sclerosis (MS) is a demyelinating disease in which an inflammatory cell infiltrate represents a characteristic pathologic feature of active lesions within the CNS. The possibility has been raised that cell-mediated immune mechanisms orchestrate the pathogenesis of MS. Cytokines play a particularly important role in cellular immune mechanisms. These soluble glycoproteins, nonimmunoglobulin in nature, act nonenzymatically to regulate immune cell function. A unique family of cytokines, the tumor necrosis factors (TNFs), demonstrate immunoregulatory activity but are also involved in the effector arm of cellular immune responses. Recently, studies both in vitro and in vivo have suggested a role for TNFs in the pathology of MS. This report summarizes data implicating TNFs in the mechanisms of MS and attempts to apply the anti-TNF approach in the future therapeutic strategy for this disease.

Published
1995
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41. Tumor necrosis factor mediates myelin and oligodendrocyte damage in vitro.

Author

Selmaj KW and Raine CS

Subjects
Animals, Cells, Cultured, Interferon-gamma pharmacology, Interleukin-2 pharmacology, Mice, Myelin Sheath pathology, Myelin Sheath ultrastructure, Oligodendroglia pathology, Oligodendroglia ultrastructure, Recombinant Proteins, Myelin Sheath drug effects, Neuroglia drug effects, Oligodendroglia drug effects, Spinal Cord cytology, Tumor Necrosis Factor-alpha pharmacology
Abstract

Recombinant human tumor necrosis factor (rhTNF) has been tested for its effect on myelinated cultures of mouse spinal cord tissue. As controls, recombinant human interferon gamma (rhIFN) and interleukin-2 (rhIL-2) were tested, as well as T-cell supernatants, antigalactocerebroside serum, and normal culture medium. It was found that rhTNF induced delayed-onset (18-24 hr) oligodendrocyte necrosis and a type of myelin dilatation peculiar to this system. Some nerve fibers progressed to demyelination by 72 hours. The myelin dilatation was not reversible by return to normal feeding solution for 3 days. In contrast, rhIFN, rhIL-2, T-cell supernatants, and normal medium had little or no effect on cultures. This mechanism differs from other immune-mediated mechanisms in that it appears that a physiological (not structural) demyelination occurs initially without overt destruction of the myelin sheath. These observations are relevant to the evolution of the multiple sclerosis plaque: dysfunction of ionic channels might contribute to the eventual demise of oligodendrocytes and axons in the longstanding lesion.

Published
1988
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