7 results on '"McFarland, H. F."'
Search Results
2. Humanized anti-CD25 (daclizumab) inhibits disease activity in multiple sclerosis patients failing to respond to interferon
- Author
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Martin, R., Bielekova, B., Ohayon, J., McCartin, J., Richert, N., McFarland, H. F., Howard, T., Markovic-Plese, S., Wurfel, J., Waldmann, T. A., and Blevins, G.
- Abstract
Identifying effective treatment combinations for MS patients failing standard therapy is an important goal. We report the results of a phase II open label baseline-to-treatment trial of a humanized monoclonal antibody against CD25 (daclizumab) in 10 multiple sclerosis patients with incomplete response to IFN-β therapy and high brain inflammatory and clinical disease activity. Daclizumab was very well tolerated and led to a 78% reduction in new contrast-enhancing lesions and to a significant improvement in several clinical outcome measures.
- Published
- 2004
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3. Oral interferon beta-1a in relapsing-remitting multiple sclerosis: A double-blind randomized study
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Polman, C., Barkhof, F., Kappos, L., Pozzilli, C., Sandbrink, R., Dahlke, F., Jakobs, P., Lorenz, A., Hern, J., Coleman, R., Soelberg Srensen, P., Hartung, H. P., Fredrikson, S., Selmaj, K., Pelletier, J., D'Hooghe, M. B., Comi, G., Hohfeld, R., Gold, R., Panelius, M., Ruutiainen, J., Clanet, M., de Vos, M., Jonker, M., van Ijken, T., Jansen, E., van Schijndel, R., Karas, G., Wagner, K., Ghazi, M., Kurth, D., Sauerbrey, K., Tries, E., McFarland, H. F., Miller, D. H., Montalban, X., Petkau, J., Neurology, Radiology and nuclear medicine, and VU University medical center
- Subjects
Adult ,Male ,medicine.medical_specialty ,Adolescent ,Placebo-controlled study ,Administration, Oral ,Physical examination ,Placebo ,law.invention ,03 medical and health sciences ,0302 clinical medicine ,Multiple Sclerosis, Relapsing-Remitting ,Randomized controlled trial ,Adjuvants, Immunologic ,Double-Blind Method ,law ,Internal medicine ,medicine ,Humans ,030212 general & internal medicine ,medicine.diagnostic_test ,business.industry ,Multiple sclerosis ,Interferon beta-1a ,Interferon-beta ,Middle Aged ,medicine.disease ,Surgery ,Clinical trial ,Treatment Outcome ,Neurology ,Tolerability ,Female ,Neurology (clinical) ,business ,030217 neurology & neurosurgery ,medicine.drug - Abstract
Background: Interferon beta (IFNB) is available in parenter al formulations for treatment of multiple sclerosis (MS). The purpo se of this study was to evaluate safety, tolerability and effects on MRI lesions of three different doses of oral IFNB-1a compared with placebo over six months in relapsing-remitting (RR) MS patients. Methods: In this multicenter, double-blind randomized trial, RR -MS patients received 0.06, 0.6 or 6 million international units (MIU) IFNB-1a or placebo every other day for up to six months. G adolinium DTPA enhanced brain MRI scans were performed at screening and monthly during treatment. The primary variable was the cumulative number of newly active lesions. Secondary variables included volume of enhancing lesions on T1-weighted images each month and lesion volume on T2-weighted images at months three and six. Safety measures included adverse events, laboratory variables, vital signs, ECG, physical examination, EDSS and number of relapses. Neopterin was measured in 21 patients and neutralizing antibodies in 24 patients. Results: O f 194 screened patients, 173 were randomized (42-44 patients per group) in 15 centers. Median cumulative numbers of newly active lesions over six months were 4.0 in the placebo and 0.6 MIU groups, compared with 7.5 and 9.0 in the 0.06 and 6 MIU groups (no significant differences). Secondary efficacy endpoints showed small and inconsistent differences between groups. A dverse events showed no notable group differences. A pproximately two-thirds of patients in each group remained relapse free. No patients showed neutralizing antibodies. Neopterin levels were comparable between groups. Conclusion: O ral IFNB-1a showed neither beneficial effects in RRMS nor any systemic biological effects. Treatment was safe and well tolerated.
- Published
- 2003
4. HLA restriction and TCR usage of T lymphocytes specific for a novel candidate autoantigen, X2 MBP, in multiple sclerosis
- Author
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Voskuhl, R. R., Robinson, E. D., Benjamin Segal, Tranquill, L., Camphausen, K., Albert, P. S., Richert, J. R., and Mcfarland, H. F.
- Subjects
Immunology ,Immunology and Allergy - Abstract
Previous investigations of the major 18.5-kDa isoform of myelin basic protein (MBP) as a target autoantigen in multiple sclerosis (MS) have failed to identify an epitope uniformly recognized with higher frequency in MS patients compared with controls. Because remyelination has been observed in MS plaques, we were prompted to investigate T cells specific for myelin protein isoforms with up-regulated expression during remyelination. We have recently described such T cells that recognize the exon 2-encoded region of MBP (X2 MBP), a sequence included in the 21.5- and 20.2-kDa isoforms of MBP. These cells were shown to be CD4+, HLA class II restricted, and cytolytic. In members of one multiplex MS family, X2 MBP-specific T lymphocytes were as prevalent as T cells specific for immunodominant regions within the major 18.5-kDa isoform of MBP. The present study characterizes X2 MBP-specific T cell responses in additional multiplex MS family members as well as in heterogeneous (non-familial) MS patients and in healthy controls. The frequencies of X2 MBP-specific T cells in each of the affected family members from two of three MS families were significantly increased as compared with both the heterogeneous MS group and the healthy control group. Also, X2 MBP-specific T cell lines from affected family members were primarily restricted to molecules encoded by the DR2/DQw1 allele. Although TCR usage was generally heterogeneous, there was evidence of intraindividual sequence identity. These data suggest that: 1) Myelin proteins with up-regulated expression during the course of disease should be considered as candidate autoantigens in MS. 2) The functional basis for the association of DR2/DQw1 inheritance with MS susceptibility may be related to presentation of autoantigens by this allele. 3) TCR therapy will need to be individually tailored to target the most prevalent autoantigen-specific response.
5. The role of autoimmune t lymphocytes in the pathogenesis of multiple sclerosis
- Author
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Hohlfeld, R., Meinl, E., Weber, F., Zipp, F., Schmidt, S., Sotgiu, S., Goebels, N., Voltz, R., Spuler, S., Iglesias, A., Wekerle, H., Staudt, L. M., Lenardo, M. J., Matis, L. A., Germain, R. N., Margulies, D. H., Bjorkman, P. J., Saper, M. A., Samraoui, B., Brown, J. H., Jardetzky, T. S., Gorga, J. C., Ben-Nun, A., Cohen, I. R., Toyka, K. V., Heininger, K., Drexler, K., Fleckenstein, B., Allegretta, M., Nicklas, J. A., Sriram, S., Albertini, R. J., Ofosu-Appiah, W., Mokhtarian, F., Miller, A., Grob, D., Zhang, J., Markovic, S., Lacet, B., Oksenberg, J. R., Panzara, M. A., Begovich, A. B., Kojima, K., Lannes-Vieira, J., Lassmann, H., Fritz Zimprich, Rossler, K., Berger, T., Wucherpfennig, K. W., Weiner, H. L., Hafler, D. A., Martin, R., Mcfarland, H. F., Mcfarlin, D. E., Uematsu, Y., Wege, H., Straus, A., Salvetti, M., Ristori, G., D Amato, M., Witek, C., Selmaj, K., Brosnan, C. F., Raine, C. S., Battistini, L., Kowal, C., Arnason, B. G. W., Steinman, L., Medaer, R., Stinissen, P., Bourdette, D. N., Whitham, R. H., Chou, Y. K., and Friedman, A.
6. Circulating adhesion molecules and inflammatory mediators in demyelination: A review
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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.
7. In vivo detection of cortical plaques by MR imaging in patients with multiple sclerosis
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Bagnato, F., Butman, J. A., Gupta, S., Calabrese, M., Lukas Pezawas, Ohayon, J. M., Tovar-Moll, F., Riva, M., Cao, M. M., Talagala, S. L., and Mcfarland, H. F.
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