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121. Cell-associated subacute sclerosing panencephalitis agent studied in organotypic central nervous system cultures: viral rescue attempts and morphology

Author

Sheppard, R D, Raine, C S, Burnstein, T, Bornstein, M B, and Feldman, L A

Abstract

Organotypic cultures of hamster cerebellum were exposed to the IP-3-Ca cell line , which contains a cell-associated subacute sclerosing panencephalitis agent. Central nervous system (CNS) cultures were examined by light and electron microscopy as well as standard virological techniques from 3 to 46 days postinfection. The results indicate that although viral nucleocapsid material was transferred to elements of the CNS, cell-free virus could not be detected by virological techniques and by electron microscopy, and budding viral particles were not observed. Attempts to recover cell-free virus from hamster CNS tissue exposed to IP-3-Ca cells were generally negative. However, 2% of the cultures yielded low levels of infectious virus. IP-3-Ca cells were able to transfer the cell-associated viral material to all cell types found in the CNS cultures and were capable of inducing polykaryocytes in the CNS cultures. The role of cell-associated virus-like agents in subacute sclerosing panencephalitis and other chronic CNS infections is discussed.

Published
1975
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122. Rapid degradation restricts measles virus matrix protein expression in a subacute sclerosing panencephalitis cell line.

Author

Sheppard, R D, Raine, C S, Bornstein, M B, and Udem, S A

Abstract

Measles virus matrix protein expression is restricted in the persistently infected brain cells of patients with the chronic neurological disease subacute sclerosing panencephalitis (SSPE). Prior studies of the nature of this restriction have identified polyadenylylated matrix gene-encoded RNA transcripts unable to direct effective translation. The defective nature of these mRNAs readily accounted for the inability to detect matrix protein in these persistently infected cells and suggested that in SSPE the restriction of matrix protein expression is achieved by preventing its synthesis. Recently, however, we reported evidence that matrix protein is synthesized in at least one example of this persistent infection, the SSPE cell line IP-3-Ca. In this case, failure of matrix protein to accumulate normally accounted for its restricted expression [Sheppard, R. D., Raine, C. S., Bornstein, M. B. & Udem, S. A. (1985) Science 228, 1219-1221]. To clarify the nature of the restriction displayed by IP-3-Ca cells, the synthesis and fate of the matrix protein of this SSPE cell line were examined in detail. No evidence of constraints on the efficiency of matrix protein mRNA transcription or translation was found. Instead, the restricted expression proved to be the result of rapid posttranslational degradation of matrix protein. We suggest that matrix protein gene mutations incurred in the course of genome replication are likely to be responsible for the diversity of observed mechanisms restricting matrix protein expression. In that event, the nature and position of the nucleotide substitution(s) would be the determinants of the level at which restricted expression is achieved.

Published
1986
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124. Clonal expansion and decreased occurrence of peripheral blood gamma delta T cells of the V delta 2J delta 3 lineage in multiple sclerosis patients.

Author

Liedtke, W, Meyer, G, Faustmann, P M, Warnatz, H, and Raine, C S

Abstract

gamma delta T cells are implicated in autoimmune diseases but their precise function remains unclear. In multiple sclerosis (MS) brain tissue, gamma delta T cells co-localize with heat shock protein (hsp)65+ oligodendrocytes and are oligoclonally restricted in the V delta 2J delta 3 lineage. To investigate the homing properties and the degree of heterogeneity of V delta 2J delta 3+ gamma delta T cells in MS, peripheral blood lymphocytes (PBL) from 34 MS patients, 42 controls (14 autoimmune control patients, 28 healthy volunteers), and 11 lymphatic tissues of MS patients and controls were studied by RT-PCR and sequencing. V delta 2J delta 3 TCR rearrangement was detected in 27 out of 28 healthy controls, and was significantly less frequent in MS patients (24 out of 34) and autoimmune control patients (seven out of 14). It was present only in five out of 11 tissue specimens, none of them from MS patients. Direct sequencing and cloning/automated sequencing of the V delta 2J delta 3 PCR products indicated heterogeneity in healthy controls and oligoclonality in MS patients, but also in autoimmune control patients. Differences between MS patients and healthy controls were more accentuated in exacerbating hospitalized patients than in clinically stable outpatients participating in a clinical trial. Only one V delta 2J delta 3 sequence of a total of 85 different sequences obtained was shared between two MS patients. Taken together, evidence for clonal expansion of V delta 2J delta 3+ gamma delta T cells was found in PBL of MS patients. This T cell subset, previously shown to be present in 100% of chronic-active MS plaques, might home to the CNS in MS, resulting in its under-representation in the blood.

Published
1997
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125. Ultrastructure of Measles Virus in Cultures of Hamster Cerebellum

Author

Raine, C. S., Feldman, L. A., Sheppard, R. D., and Bornstein, M. B.

Abstract

Replication of Edmonston strain of measles virus in cultures of hamster central nervous system tissue was studied by electron microscopy of ultrathin sections. Infected cultures were fixed from 3 hr to 39 days postinoculation (PI). Measles nucleocapsid was first seen within the cytoplasm of giant cells, the latter appearing 5 to 6 days PI. Measles virus particles were most abundant at 10 days PI and appeared to bud off from areas of the cell membrane along which nucleocapsid was aligned. Intranuclear nucleocapsid was more abundant at later stages, and by 39 days PI entire nuclei were seen to be occupied. By this time, the cytoplasmic formations, which had been sequestered by membranes, appeared to lose their regular structure. Budding viral particles at 39 days PI were of a much simplified structure and did not involve the alignment of nucleocapsid about their periphery.

Published
1969
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129. Cytokine localization in multiple sclerosis lesions: Correlation with adhesion molecule expression and reactive nitrogen species

Author

Brosnan, C. F., Cannella, B., Battistini, L., Raine, C. S., Mosmann, T. R., Coffman, R. L., Selmaj, K., Benveniste, E. N., Hofman, F. M., Hanwehr, R. I., Dinarello, C. A., Woodroofe, M. N., Bellamy, A. S., Feldman, M., Cuzner, M. L., Hinton, D. R., Johnson, K., Merrill, J. E., Pober, J. S., Martiney, J. A., Litwak, M., Berman, J. W., Jacobs, C. A., Baker, P. E., Roux, E. R., Lee, S. C., Liu, W., Dickson, D. W., Hurwitz, A. A., Lyman, W. D., Guida, M. P., Schroeder, C. E., Ruddle, N. H., Bergman, C. M., Mcgrath, M. L., Cross, A. H., Barten, D. M., Traugott, U., Lebon, P., Merill, J. E., Simmons, R. D., Willenborg, D. O., Racke, M. K., Bonomo, A., Scott, D. E., Paul, W. E., Seder, R. A., Moore, K. W., Waal Malefyt, R., Abrams, J., Bennett, B., Fiorentino, D. F., Zlotnik, A., Oswald, I. P., Wynn, T. A., Sher, A., James, S. L., Kennedy, M. K., Torrance, D. S., Picha, K. S., Mohler, K. M., Chen, Y., Kuchroo, V. K., Inobe, J. -I, Bogdan, C., Paik, J., Vodovotz, Y., Nathan, C., Dubois, C. M., Ruscetti, F. W., Palaszynski, E. W., Gamble, J. R., Vadas, M. A., Dhib-Jalbut, S., Johns, L. D., Flanders, K. C., Ranhes, G. E., Sriram, S., Kuruvilla, A. P., Shah, R., Hochwald, G. M., Dinther-Janssen, A. C. H. M., Horst, R., Koopman, G., Zheng, Y. M., Schafer, E., Macmicking, J. D., Weidemann, M. J., Lin, R. F., Lin, T. S., Tilton, R. G., Misko, T. P., Murphy, S., Simmons, M. L., Agullo, L., Zembala, M., Maciej Siedlar, Marcinkiewicz, J., Pryjma, J., Tada, T., Ohzeki, S., and Utsumi, K.

132. 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.

133. Cell Death during Autoimmune Demyelination: Effector but Not Target Cells Are Eliminated by Apoptosis

Author

Bruno BONETTI, Pohl, J., Gao, Y. -L, and Raine, C. S.

Subjects
Immunology, Immunology and Allergy
Abstract

The Fas and FasL apoptotic pathway was investigated by protein immunohistochemistry, flow cytometry, and reverse transcriptase-PCR analysis to assess whether it is involved in the elimination of target and/or effector cells from the central nervous system (CNS) during adoptively transferred chronic relapsing experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis. In addition to Fas and FasL, we studied Bax, an intracellular protein of the apoptotic cascade, the Bax antagonist and anti-apoptotic molecule Bcl-2, and DNA fragmentation, the final step in the apoptotic pathway. Infiltrating CD4+ T cells and parenchymal microglia expressed Fas, FasL, and Bax, and about half of these cells showed DNA fragmentation, a combination indicative of ongoing apoptosis. Using flow cytometry and reverse transcriptase-PCR, a positive correlation was seen between disease activity and up-regulation of the Fas system; in fact, Fas and FasL were expressed at low levels at the onset of EAE and increased at the height of disease to involve about one-third of all infiltrating lymphocytes. In the normal CNS, Fas immunoreactivity was constitutively present at low levels on oligodendrocytes and was up-regulated in the CNS during the course of EAE. However, oligodendrocytes showed no Bax reactivity or DNA fragmentation and expressed high levels of Bcl-2, as did the majority of infiltrating CD3+ cells, a pattern inconsistent with apoptosis. Thus, while molecules of the apoptotic cascade are well represented in the CNS during EAE, their expression correlates with elimination of infiltrating cells and microglia, not the myelinating cell, the oligodendrocyte.

135. The role of autoimmune t lymphocytes in the pathogenesis of multiple sclerosis

Author

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.

136. Cytokine production in the central nervous system

Author

Woodroofe, M. N., Dantzer, R., Gutierrez, E. G., Banks, W. A., Kastin, A. J., Ortiz, L., Plotkin, S. R., Farrar, W. L., Kilian, P. L., Ruff, M. R., Blatteis, C. M., Gatti, S., Bartfai, T., Frei, K., Lius, H., Schmedel, C., Fontana, A., Daniel B. Constam, Phillipp, J., Malipiero, K. V., Sarna, G. S., Wadhwa, M., Loughlin, A. J., Cuzner, M. L., Selmaj, K., Raine, C. S., Honegger, P., Giulian, D., Woodward, J., Young, D. G., Mcclain, C. J., Cohen, D., Ott, L., Nuovo, G. J., Gallery, F., Macconnell, P., and Brown, A.

137. 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.

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