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17. Polymorphous low-grade neuroepithelial tumor of the young (PLNTY): an epileptogenic neoplasm with oligodendroglioma-like components, aberrant CD34 expression, and genetic alterations involving the MAP kinase pathway

Author

Huse, JT, Snuderl, M, Jones, DTW, Brathwaite, CD, Altman, N, Lavi, E, Saffery, R, Sexton-Oates, A, Blumcke, I, Capper, D, Karajannis, MA, Benayed, R, Chavez, L, Thomas, C, Serrano, J, Borsu, L, Ladanyi, M, Rosenblum, MK, Huse, JT, Snuderl, M, Jones, DTW, Brathwaite, CD, Altman, N, Lavi, E, Saffery, R, Sexton-Oates, A, Blumcke, I, Capper, D, Karajannis, MA, Benayed, R, Chavez, L, Thomas, C, Serrano, J, Borsu, L, Ladanyi, M, and Rosenblum, MK

Abstract

Epileptogenic tumors affecting children and young adults are a morphologically diverse collection of neuroepithelial neoplasms that, as a group, exhibit varying levels of glial and/or neuronal differentiation. Recent advances in molecular profiling technology, including comprehensive DNA sequencing and methylation analysis, have enabled the application of more precise and biologically relevant classification schemes to these tumors. In this report, we describe a morphologically and molecularly distinct epileptogenic neoplasm, the polymorphous low-grade neuroepithelial tumor of the young (PLNTY), which likely accounts for a sizable portion of oligodendroglioma-like tumors affecting the pediatric population. Characteristic microscopic findings most notably include infiltrative growth, the invariable presence of oligodendroglioma-like cellular components, and intense immunolabeling for cluster of differentiation 34 (CD34). Moreover, integrative molecular profiling reveals a distinct DNA methylation signature for PLNTYs, along with frequent genetic abnormalities involving either B-Raf proto-oncogene (BRAF) or fibroblast growth factor receptors 2 and 3 (FGFR2, FGFR3). These findings suggest that PLNTY represents a distinct biological entity within the larger spectrum of pediatric, low-grade neuroepithelial tumors.

Published
2017

23. Antibodies against IL-12 prevent superantigen-induced and spontaneous relapses of experimental autoimmune encephalomyelitis

Author

Cris Constantinescu, Wysocka, M., Hilliard, B., Ventura, E. S., Lavi, E., Trinchieri, G., and Rostami, A.

Subjects
Male, Staphylococcus aureus, Encephalomyelitis, Autoimmune, Experimental, Immunology, Guinea Pigs, Severity of Illness Index, Autoimmune Diseases, Enterotoxins, Mice, Recurrence, Immunology and Allergy, Animals, Inflammation, Antigens, Bacterial, Superantigens, Molecular Mimicry, Antibodies, Monoclonal, Brain, Myelin Basic Protein, Th1 Cells, Interleukin-12, Rats, Spinal Cord, Cytokines, Female, Immunization, Demyelinating Diseases
Abstract

Immunization of (PL/J × SJL/J)F1 mice with myelin basic protein (MBP) induces relapsing experimental autoimmune encephalomyelitis (EAE). Relapses occur 7 to 10 days after recovery from the initial paralysis. Staphylococcal enterotoxins (SE) A or B, administered after recovery from the initial paralysis, induce immediate relapses. IL-12 is involved in the induction of EAE. Here, we show that SEA and SEB induce IL-12 in splenocytes from (PL/J × SJL/J)F1 mice in vitro and increase the level of IL-12 in the sera of mice treated with these superantigens. IL-12 administration mimics SE in inducing spontaneous relapses and in enhancing the severity and frequency of spontaneous relapses. IL-12 neutralization blocks SE-induced and subsequent relapses of EAE, and, when instituted after recovery from the initial attack, prevents spontaneous relapse. This is the first report of prevention of relapses of EAE with anti-IL-12 Ab, an approach which may prove useful in the prevention of exacerbations in multiple sclerosis.

Published
1998

24. CXCR-4 (Fusin), a co-receptor for the type 1 human immunodeficiency virus (HIV-1), is expressed in the human brain in a variety of cell types, including microglia and neurons

Author

Lavi, E., Strizki, J. M., Ulrich, A. M., Zhang, W., Fu, L., Wang, Q., O'Connor, M., Hoxie, J. A., and González-Scarano, F.

Subjects
Adult, Male, Neurons, Receptors, CXCR4, AIDS Dementia Complex, Antibodies, Monoclonal, Brain, Middle Aged, Immunohistochemistry, Polymerase Chain Reaction, HIV-1, Humans, Female, Microglia, RNA, Messenger, Cells, Cultured, In Situ Hybridization, Research Article, Aged, DNA Primers
Abstract

Entry of the type 1 human immunodeficiency virus into most cells requires the presence of the CD4 protein in combination with one of several recently described co-receptors. CXCR-4 (fusin) was the first identified, and it serves as co-receptor for T-cell-line tropic (T-tropic) HIV-1 isolates. To determine the expression of CXCR-4 in the brain, a major target of HIV pathology, we used immunohistochemistry and reverse transcriptase polymerase chain reaction with CXCR-4-specific antibodies and probes. We found that CXCR-4 was expressed in several cell types in brain, but notably in neurons and microglia, a finding that was replicated in tissue culture. The study of the expression of CXCR-4 in the brain, which may be one of many chemokine receptors in the central nervous system, may provide further insight into the interactions between brain cells, pathogens, and the immune system, and help understand the pathogenesis of HIV dementia.

Published
1997

26. Apolipoprotein(a) deposition in atherosclerotic plaques of cerebral vessels. A potential role for endothelial cells in lesion formation

Author

Jamieson, D. G., Usher, D. C., Rader, D. J., and Lavi, E.

Subjects
Adult, Aged, 80 and over, Male, Arteriosclerosis, Cerebral Arteries, Middle Aged, Apoprotein(a), Immunohistochemistry, Apolipoproteins, cardiovascular system, Humans, Female, Endothelium, Vascular, Research Article, Aged, Lipoprotein(a)
Abstract

Atherosclerosis is the leading cause of death and serious morbidity in economically developed societies through its sequelae of coronary artery and cerebrovascular disease. The causes and mechanisms of atherosclerosis are still largely unknown. Serum levels of a lipoprotein, Lp(a), have been shown, in retrospective and some prospective clinical studies, to be associated with increased risk of myocardial and cerebral infarction. The active part of Lp(a), apo(a), has > 80% homology with plasminogen; thus it may competitively inhibit the thrombolytic action of plasminogen and enhance thrombogenesis. Lp(a) has been shown to be deposited in the vascular wall of the aorta and coronary vessels, but its presence in the cerebral vessels has not yet been shown. Autopsy specimens of vessels of the circle of Willis from 23 patients were examined for degree of atherosclerosis and deposition of apo(a) by immunohistochemistry with apo(a)-specific monoclonal antibodies. The amount of apo(a) deposition in cerebral vessels correlated well with the degree of cerebral atherosclerosis. Arterial deposition of apo(a) was found entirely within the endothelial cell and subendothelial cell layers. There was no staining within the media and adventitia, with the exception of staining within the endothelial cells of the vasa vasorum. Correlation between the morphology of apo(a) deposition and plaque stage was found suggesting that detection of apo(a) in endothelial cells is an early event in the development of the atherosclerotic plaque of cerebral vessels.

Published
1995

27. A mucin-like glycoprotein identified by MAG (mouse ascites Golgi) antibodies. Menstrual cycle-dependent localization in human endometrium

Author

Harvey Kliman, Feinberg, R. F., Schwartz, L. B., Feinman, M. A., Lavi, E., and Meaddough, E. L.

Subjects
Adult, Male, Mice, Inbred BALB C, Immunoblotting, Molecular Sequence Data, Mucins, Golgi Apparatus, ABO Blood-Group System, Immunoenzyme Techniques, Endometrium, Epitopes, Mice, nervous system, Carbohydrate Sequence, Lectins, Blood Group Antigens, Animals, Ascitic Fluid, Humans, Female, Menstrual Cycle, Research Article, Glycoproteins
Abstract

Human endometrial glands synthesize and secrete a high molecular weight mucin-like glycoprotein in a menstrual cycle-dependent fashion. A novel moiety within this Golgi-associated glycoprotein is strongly reactive with IgG antibodies in numerous murine ascites, and has been termed MAG (mouse ascites Golgi). Immunohistochemical staining of 201 endometrial biopsies revealed the following patterns: MAG first appeared in the Golgi on cycle day 5, peaked on day 15, was present on the surface of the luminal epithelium between days 17 and 19, and was no longer detectable after day 19. MAG was also present in cervical, prostate, seminal vesicle, and lacrimal glands, pancreatic acinar cells, gall bladder and bile duct epithelium, and certain cells of the salivary and sweat glands. Interestingly, only tissues from blood group A individuals exhibited this staining. As a common link among all these cell types is the expression of mucins, we speculated that the MAG epitope could be a mucin-associated blood group A-related epitope. This hypothesis was tested by absorption experiments with a variety of glycoconjugates and erythrocytes and by immunoblots of MAG-rich material. The absorption studies demonstrated that only type III porcine mucin (< 1% sialic acid) and blood type A or AB erythrocytes were able to absorb the anti-MAG antibody. Inasmuch as N-acetyl-galactosamine alone, the terminal blood group A carbohydrate, did not block MAG antibody binding, the MAG epitope appears to involve N-acetylgalactosamine plus other determinants. Immunoblots of endometrial extracts and saliva from blood type A individuals revealed MAG-reactive material with a molecular weight > 200 kd under reducing conditions. Because the MAG epitope appears on the endometrial surface during the purported implantation window, we speculate that mucin-like epitopes could play a role in the earliest apposition phases of conceptus-endometrial interaction.

Published
1995

28. RADIATION THERAPY

Author

Behera, M. K., primary, Sharma, A., additional, Dutta, S., additional, Sharma, S., additional, Julka, P. K., additional, Rath, G. K., additional, Kil, W. J., additional, Ko, C., additional, Kaushal, A., additional, Warran, K., additional, Ning, H., additional, Camphausen, K., additional, Smart, D., additional, Vern-Gross, T. Z., additional, McMullen, K. P., additional, Case, L. D., additional, Bourland, J. D., additional, Ellis, T. L., additional, Lawrence, J. A., additional, Tatter, S. B., additional, Shaw, E. G., additional, Urbanic, J. J., additional, Chan, M. D., additional, Jensen, R. L., additional, Shrieve, D. C., additional, Mohindra, P., additional, Robins, H. I., additional, Tome, W. A., additional, Howard, S. P., additional, Chen, C., additional, Damek, D., additional, Gaspar, L. E., additional, Ney, D., additional, Waziri, A., additional, Lillehei, K., additional, Kavanagh, B. D., additional, Wang, C.-C., additional, Floyd, S., additional, Chang, C.-H., additional, Warnke, P., additional, Chio, C.-C., additional, Kasper, E., additional, Mahadevan, A., additional, Wong, E., additional, Jeyapalan, S., additional, Mahajan, A., additional, Grosshans, D., additional, McAleer, M. F., additional, Brown, P. D., additional, Chintagumpala, M., additional, Vats, T., additional, Puduvalli, V., additional, Yock, T., additional, Schulder, M., additional, Herschmann, Y., additional, Ghaly, M., additional, Knisely, J., additional, Kapur, A., additional, Goetz, P., additional, Lwu, S., additional, Ebinu, J., additional, Arayee, M., additional, Monsalves, E., additional, Laperriere, N., additional, Menard, C., additional, Bernstein, M., additional, Zadeh, G., additional, Loganathan, A. G., additional, Alphonse, N., additional, Peiffer, A. M., additional, Johnson, A., additional, Saconn, P. A., additional, Munley, M. T., additional, Aryaee, M., additional, Lowe, C., additional, DeGroot, J., additional, Mark, G., additional, Ruda, R., additional, Trevisan, E., additional, Magliola, U., additional, Bertero, L., additional, Bosa, C., additional, Ricardi, U., additional, Soffietti, R., additional, Rajappa, P., additional, Margetis, K., additional, Wernicke, A. G., additional, Sherr, D. L., additional, Lavi, E., additional, Fine, R. L., additional, Schwartz, T., additional, Pannullo, S. C., additional, Laack, N., additional, Blanchard, M., additional, Buckner, J., additional, Glass, J., additional, Andrews, D. W., additional, Werner-Wasik, M., additional, Evans, J., additional, Lawrence, Y. R., additional, Shi, W., additional, Strauss, I., additional, Corn, B. W., additional, Matceyevsky, D., additional, Alani, S., additional, Gez, E., additional, Shtraus, N., additional, Kanner, A. A., additional, Spasic, M., additional, Choy, W., additional, Nagasawa, D., additional, Yang, I., additional, Noel, M., additional, Woolf, E., additional, Smith, R., additional, Castillo-Rojas, P., additional, Sorenson, S., additional, Smith, K., additional, Scheck, A. C., additional, Han, S. J., additional, Oh, M. C., additional, Sughrue, M. E., additional, Rutkowski, M. J., additional, Aranda, D., additional, Barani, I. J., additional, Parsa, A. T., additional, Redmond, K. J., additional, Horska, A., additional, Ishaq, O., additional, Ford, E., additional, McNutt, T., additional, Batra, S., additional, Kleinberg, L., additional, Wharam, M., additional, Mahone, M., additional, Terezakis, S., additional, Ryu, S., additional, Rock, J., additional, Movsas, B., additional, Mikkelsen, T., additional, Rosenblum, M., additional, Sabsevitz, D., additional, Bovi, J. A., additional, Leo, P., additional, LaViolette, P., additional, Rand, S., additional, Mueller, W., additional, Phillips, A., additional, Venkatramani, R., additional, Olch, A., additional, Grimm, J., additional, Davidson, T., additional, Brown, R., additional, Dhall, G., additional, Finlay, J., additional, and Wong, K., additional

Published
2011
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31. Role of CCR5 in infection of primary macrophages and lymphocytes by macrophage-tropic strains of human immunodeficiency virus: resistance to patient-derived and prototype isolates resulting from the delta ccr5 mutation

Author

Rana, S, Besson, G, Cook, D G, Rucker, J, Smyth, R J, Yi, Y, Turner, John, Guo, H H, Du, J G, Peiper, S C, Lavi, E, Samson, M, Libert, Frédérick, Liesnard, Corinne, Vassart, Gilbert, Doms, Robert W., Parmentier, Marc, Collman, R G, Rana, S, Besson, G, Cook, D G, Rucker, J, Smyth, R J, Yi, Y, Turner, John, Guo, H H, Du, J G, Peiper, S C, Lavi, E, Samson, M, Libert, Frédérick, Liesnard, Corinne, Vassart, Gilbert, Doms, Robert W., Parmentier, Marc, and Collman, R G

Abstract

The alpha-chemokine receptor fusin (CXCR-4) and beta-chemokine receptor CCR5 serve as entry cofactors for T-cell (T)-tropic and macrophage (M)-tropic human immunodeficiency virus type 1 (HIV-1) strains, respectively, when expressed with CD4 in otherwise nonpermissive cells. Some M-tropic and dual-tropic strains can also utilize other beta-chemokine receptors, such as CCR2b and CCR3. A mutation of CCR5 (delta ccr5) was recently found to be common in certain populations and appears to confer protection against HIV-1 in vivo. Here, we show that this mutation results in a protein that is expressed intracellularly but not on the cell surface. Primary CD4 T cells from delta ccr5 homozygous individuals were highly resistant to infection with prototype M-tropic HIV-1 strains, including an isolate (YU-2) that uses CCR5 and CCR3, but were permissive for both a T-tropic strain (3B) and a dual-tropic variant (89.6) that uses CXCR-4, CCR5, CCR3, or CCR2b. These cells were also resistant to M-tropic patient isolates but were readily infected by T-tropic patient isolates. Primary macrophages from delta ccr5 homozygous individuals were also resistant to infection with M-tropic strains, including YU-2, but the dual-tropic strain 89.6 was able to replicate in them even though macrophages are highly resistant to CXCR-4-dependent T-tropic isolates. These data show that CCR5 is the essential cofactor for infection of both primary macrophages and T lymphocytes by most M-tropic strains of HIV-1. They also suggest that CCR3 does not function for HIV-1 entry in primary lymphocytes or macrophages, but that a molecule(s) other than CCR5 can support entry into macrophages by certain virus isolates. These studies further define the cellular basis for the resistance to HIV-1 infection of individuals lacking functional CCR5., Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S., info:eu-repo/semantics/published

Published
1997

33. Mouse hepatitis virus A59-induced demyelination can occur in the absence of CD8+ T cells.

Author

Gombold, JL, Sutherland, RM, Lavi, E, Paterson, Y, Weiss, SR, Gombold, JL, Sutherland, RM, Lavi, E, Paterson, Y, and Weiss, SR

Abstract

Mouse hepatitis virus causes a chronic demyelinating disease in C57BL/6 mice. While early studies suggested demyelination is due to direct cytolytic effects of virus on oligodendrocytes, there is increasing evidence for the involvement of the immune system in the mechanism of demyelination. In this study we have asked whether demyelination can occur in the absence of functional MHC class I expression and CD8+ T cells. We infected transgenic mice lacking expression of beta 2 microglobulin (beta 2 M -/- mice) with MHV-A59. In beta 2M-/- mice, virus was much more lethal than in either of the parental strains used to produce the mice; furthermore, while clearance from the CNS did occur in beta 2M-/- mice, it was slower than in C57BL/6 mice. This is consistent with the importance of CD8+ cells in viral clearance. Because of the increased sensitivity of the beta 2M-/- mice to infection, only low levels of virus could be used to evaluate chronic disease. Even at these low levels, demyelination did occur in some animals. To compare infection in beta 2M-/- and C57BL/6 mice we used a higher dose of an attenuated variant of MHV-A59, C12. The attenuated variant induced less demyelination in C57BL/6 mice compared to wild type A59, but the levels observed were not significantly different from those seen in beta 2M-/- mice. Thus, MHV-induced demyelination can occur in some animals in the absence of MHC class I and CD8+ cells.

Published
1995

40. Role of CCR5 in infection of primary macrophages and lymphocytes by macrophage-tropic strains of human immunodeficiency virus: resistance to patient-derived and prototype isolates resulting from the delta ccr5 mutation

Author

Rana, S, primary, Besson, G, additional, Cook, D G, additional, Rucker, J, additional, Smyth, R J, additional, Yi, Y, additional, Turner, J D, additional, Guo, H H, additional, Du, J G, additional, Peiper, S C, additional, Lavi, E, additional, Samson, M, additional, Libert, F, additional, Liesnard, C, additional, Vassart, G, additional, Doms, R W, additional, Parmentier, M, additional, and Collman, R G, additional

Published
1997
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41. Reply from the Authors

Author

Hurst, R. W., primary, Kenyon, L. C., additional, Lavi, E., additional, Raps, E. C., additional, and Marcotte, P., additional

Published
1996
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