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Journal articles on the topic 'EBI2'

Author: Grafiati

Published: 4 June 2021

Last updated: 4 February 2022

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1

Velasco-Estevez, Maria, Nina Koch, Ilona Klejbor, Stephane Laurent, Kumlesh K. Dev, Andrzej Szutowicz, Andreas W. Sailer, and Aleksandra Rutkowska. "EBI2 Is Temporarily Upregulated in MO3.13 Oligodendrocytes during Maturation and Regulates Remyelination in the Organotypic Cerebellar Slice Model." International Journal of Molecular Sciences 22, no. 9 (April 21, 2021): 4342. http://dx.doi.org/10.3390/ijms22094342.

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The EBI2 receptor regulates the immune system and is expressed in various immune cells including B and T lymphocytes. It is also expressed in astrocytes in the central nervous system (CNS) where it regulates pro-inflammatory cytokine release, cell migration and protects from chemically induced demyelination. Its signaling and expression are implicated in various diseases including multiple sclerosis, where its expression is increased in infiltrating immune cells in the white matter lesions. Here, for the first time, the EBI2 protein in the CNS cells in the human brain was examined. The function of the receptor in MO3.13 oligodendrocytes, as well as its role in remyelination in organotypic cerebellar slices, were investigated. Human brain sections were co-stained for EBI2 receptor and various markers of CNS-specific cells and the human oligodendrocyte cell line MO3.13 was used to investigate changes in EBI2 expression and cellular migration. Organotypic cerebellar slices prepared from wild-type and cholesterol 25-hydroxylase knock-out mice were used to study remyelination following lysophosphatidylcholine (LPC)-induced demyelination. The data showed that EBI2 receptor is present in OPCs but not in myelinating oligodendrocytes in the human brain and that EBI2 expression is temporarily upregulated in maturing MO3.13 oligodendrocytes. Moreover, we show that migration of MO3.13 cells is directly regulated by EBI2 and that its signaling is necessary for remyelination in cerebellar slices post-LPC-induced demyelination. The work reported here provides new information on the expression and role of EBI2 in oligodendrocytes and myelination and provides new tools for modulation of oligodendrocyte biology and therapeutic approaches for demyelinating diseases.

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2

Nevius, Erin, Flavia Pinho, Meera Dhodapkar, Huiyan Jin, Kristina Nadrah, Mark C. Horowitz, Junichi Kikuta, Masaru Ishii, and João P. Pereira. "Oxysterols and EBI2 promote osteoclast precursor migration to bone surfaces and regulate bone mass homeostasis." Journal of Experimental Medicine 212, no. 11 (October 5, 2015): 1931–46. http://dx.doi.org/10.1084/jem.20150088.

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Bone surfaces attract hematopoietic and nonhematopoietic cells, such as osteoclasts (OCs) and osteoblasts (OBs), and are targeted by bone metastatic cancers. However, the mechanisms guiding cells toward bone surfaces are essentially unknown. Here, we show that the Gαi protein–coupled receptor (GPCR) EBI2 is expressed in mouse monocyte/OC precursors (OCPs) and its oxysterol ligand 7α,25-dihydroxycholesterol (7α,25-OHC) is secreted abundantly by OBs. Using in vitro time-lapse microscopy and intravital two-photon microscopy, we show that EBI2 enhances the development of large OCs by promoting OCP motility, thus facilitating cell–cell interactions and fusion in vitro and in vivo. EBI2 is also necessary and sufficient for guiding OCPs toward bone surfaces. Interestingly, OCPs also secrete 7α,25-OHC, which promotes autocrine EBI2 signaling and reduces OCP migration toward bone surfaces in vivo. Defective EBI2 signaling led to increased bone mass in male mice and protected female mice from age- and estrogen deficiency–induced osteoporosis. This study identifies a novel pathway involved in OCP homing to the bone surface that may have significant therapeutic potential.

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3

Rosenkilde, Mette M., Tau Benned-Jensen, Helene Andersen, Peter J. Holst, Thomas N. Kledal, Hans R. Lüttichau, Jørgen K. Larsen, Jan P. Christensen, and Thue W. Schwartz. "Molecular Pharmacological Phenotyping of EBI2." Journal of Biological Chemistry 281, no. 19 (March 15, 2006): 13199–208. http://dx.doi.org/10.1074/jbc.m602245200.

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4

Cain, Chris. "EBI2: the race is on." Science-Business eXchange 4, no. 32 (August 2011): 895. http://dx.doi.org/10.1038/scibx.2011.895.

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5

Liu, Changlu, Xia V. Yang, Jiejun Wu, Chester Kuei, Neelakandha S. Mani, Li Zhang, Jingxue Yu, et al. "Oxysterols direct B-cell migration through EBI2." Nature 475, no. 7357 (July 2011): 519–23. http://dx.doi.org/10.1038/nature10226.

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6

Hannedouche, Sébastien, Juan Zhang, Tangsheng Yi, Weijun Shen, Deborah Nguyen, João P. Pereira, Danilo Guerini, et al. "Oxysterols direct immune cell migration via EBI2." Nature 475, no. 7357 (July 2011): 524–27. http://dx.doi.org/10.1038/nature10280.

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7

Kurschus, Florian C., and Florian Wanke. "EBI2 – Sensor for dihydroxycholesterol gradients in neuroinflammation." Biochimie 153 (October 2018): 52–55. http://dx.doi.org/10.1016/j.biochi.2018.04.014.

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8

Kerr, Jonathan. "Early Growth Response Gene Upregulation in Epstein–Barr Virus (EBV)-Associated Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)." Biomolecules 10, no. 11 (October 26, 2020): 1484. http://dx.doi.org/10.3390/biom10111484.

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Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a chronic multisystem disease exhibiting a variety of symptoms and affecting multiple systems. Psychological stress and virus infection are important. Virus infection may trigger the onset, and psychological stress may reactivate latent viruses, for example, Epstein–Barr virus (EBV). It has recently been reported that EBV induced gene 2 (EBI2) was upregulated in blood in a subset of ME/CFS patients. The purpose of this study was to determine whether the pattern of expression of early growth response (EGR) genes, important in EBV infection and which have also been found to be upregulated in blood of ME/CFS patients, paralleled that of EBI2. EGR gene upregulation was found to be closely associated with that of EBI2 in ME/CFS, providing further evidence in support of ongoing EBV reactivation in a subset of ME/CFS patients. EGR1, EGR2, and EGR3 are part of the cellular immediate early gene response and are important in EBV transcription, reactivation, and B lymphocyte transformation. EGR1 is a regulator of immune function, and is important in vascular homeostasis, psychological stress, connective tissue disease, mitochondrial function, all of which are relevant to ME/CFS. EGR2 and EGR3 are negative regulators of T lymphocytes and are important in systemic autoimmunity.

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9

Brink, Robert. "EBI2 unlocks the door to the Tfh cell nursery." Immunology & Cell Biology 94, no. 7 (June 14, 2016): 621–22. http://dx.doi.org/10.1038/icb.2016.52.

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10

Rutkowska, Aleksandra, Inga Preuss, Francois Gessier, Andreas W. Sailer, and Kumlesh K. Dev. "EBI2 regulates intracellular signaling and migration in human astrocyte." Glia 63, no. 2 (October 9, 2014): 341–51. http://dx.doi.org/10.1002/glia.22757.

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11

Barroso, Rubén, Laura Martínez Muñoz, Sergio Barrondo, Beatriz Vega, Borja L. Holgado, Pilar Lucas, Amparo Baíllo, Joan Sallés, José M. Rodríguez‐Frade, and Mario Mellado. "EBI2 regulates CXCL13‐mediated responses by heterodimerization with CXCR5." FASEB Journal 26, no. 12 (August 22, 2012): 4841–54. http://dx.doi.org/10.1096/fj.12-208876.

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12

Daugvilaite, Viktorija, Kristine Niss Arfelt, Tau Benned‐Jensen, Andreas W. Sailer, and Mette M. Rosenkilde. "Oxysterol‐EBI2 signaling in immune regulation and viral infection." European Journal of Immunology 44, no. 7 (June 20, 2014): 1904–12. http://dx.doi.org/10.1002/eji.201444493.

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13

Rutkowska, Aleksandra, Derya R. Shimshek, Andreas W. Sailer, and Kumlesh K. Dev. "EBI2 regulates pro-inflammatory signalling and cytokine release in astrocytes." Neuropharmacology 133 (May 2018): 121–28. http://dx.doi.org/10.1016/j.neuropharm.2018.01.029.

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14

Barington, L., F. Wanke, K. Niss Arfelt, P. J. Holst, F. C. Kurschus, and M. M. Rosenkilde. "EBI2 in splenic and local immune responses and in autoimmunity." Journal of Leukocyte Biology 104, no. 2 (May 9, 2018): 313–22. http://dx.doi.org/10.1002/jlb.2vmr1217-510r.

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15

Gatto, Dominique, and Robert Brink. "B cell localization: regulation by EBI2 and its oxysterol ligand." Trends in Immunology 34, no. 7 (July 2013): 336–41. http://dx.doi.org/10.1016/j.it.2013.01.007.

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16

Pereira, João P., Lisa M. Kelly, Ying Xu, and Jason G. Cyster. "EBI2 mediates B cell segregation between the outer and centre follicle." Nature 460, no. 7259 (July 13, 2009): 1122–26. http://dx.doi.org/10.1038/nature08226.

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17

Jang, M., Y. Tu, K. Kitamura, Y. Liang, T. Yamada, F. Pan, K. Tamura, H. Jiang, and T. Masunaga. "EBI2 Modulates Dendritic Cell Function to Regulate T-Cell Immune Response." Transplantation Journal 94, no. 10S (November 2012): 1126. http://dx.doi.org/10.1097/00007890-201211271-02235.

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18

Norregaard, Kristine, Tau Benned-Jensen, and Mette Marie Rosenkilde. "EBI2, GPR18, and GPR17 – Three Structurally Related but Biologically Distinct 7TM Receptors." Current Topics in Medicinal Chemistry 11, no. 6 (March 1, 2011): 618–28. http://dx.doi.org/10.2174/1568026611109060618.

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19

Wyss, Annika, Tina Raselli, Sebastian Schmidt, Kirstin Atrott, Isabelle Frey-Wagner, Christian von Mering, Andreas W. Sailer, Gerhard Rogler, and Benjamin Misselwitz. "Sa1872 EBI2 Plays a Role in the Development of Intestinal Lymphoid Structures." Gastroenterology 150, no. 4 (April 2016): S386. http://dx.doi.org/10.1016/s0016-5085(16)31361-0.

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20

Benned-Jensen, Tau, Christopher Smethurst, Peter J. Holst, Kevin R. Page, Howard Sauls, Bjørn Sivertsen, Thue W. Schwartz, Andy Blanchard, Robert Jepras, and Mette M. Rosenkilde. "Ligand Modulation of the Epstein-Barr Virus-induced Seven-transmembrane Receptor EBI2." Journal of Biological Chemistry 286, no. 33 (June 14, 2011): 29292–302. http://dx.doi.org/10.1074/jbc.m110.196345.

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21

Raselli, Tina, Annika Wyss, Kirstin Atrott, Isabelle Frey-Wagner, Andreas Geier, Andreas Sailer, Gerhard Rogler, and Benjamin Misselwitz. "Su1813 Role of Ebi2 and Oxysterols in the Pathogenesis of Fatty Liver Disease." Gastroenterology 148, no. 4 (April 2015): S—1057. http://dx.doi.org/10.1016/s0016-5085(15)33610-6.

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22

Raselli, Tina, Annika Wyss, Kirstin Atrott, Isabelle Frey-Wagner, Johannes Schmitt, Andreas Geier, Andreas Sailer, Michael Fried, Gerhard Rogler, and Benjamin Misselwitz. "Sa1716 Role of EBI2 and Oxysterols in the Pathogenesis of Fatty Liver Disease." Gastroenterology 146, no. 5 (May 2014): S—958. http://dx.doi.org/10.1016/s0016-5085(14)63488-0.

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23

Wyss, Annika, Tina Raselli, Nathan Perkins, Florian Ruiz, Gérard Schmelczer, Glynis Klinke, Anja Moncsek, et al. "The EBI2-oxysterol axis promotes the development of intestinal lymphoid structures and colitis." Mucosal Immunology 12, no. 3 (February 11, 2019): 733–45. http://dx.doi.org/10.1038/s41385-019-0140-x.

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24

Wyss, A., T. Raselli, G. Schmelczer, M. Spalinger, K. Atrott, I. Frey-Wagner, A. W. Sailer, G. Rogler, and B. Misselwitz. "P064 EBI2 and oxysterols in the development of intestinal lymphoid structures and colitis." Journal of Crohn's and Colitis 11, suppl_1 (January 26, 2017): S109—S110. http://dx.doi.org/10.1093/ecco-jcc/jjx002.190.

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25

Rutkowska, Aleksandra, Kumlesh Dev, and Andreas Sailer. "The Role of the Oxysterol/EBI2 Pathway in the Immune and Central Nervous Systems." Current Drug Targets 17, no. 16 (November 8, 2016): 1851–60. http://dx.doi.org/10.2174/1389450117666160217123042.

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26

Li, Jianhua, Erick Lu, Tangsheng Yi, and Jason G. Cyster. "EBI2 augments Tfh cell fate by promoting interaction with IL-2-quenching dendritic cells." Nature 533, no. 7601 (May 2016): 110–14. http://dx.doi.org/10.1038/nature17947.

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27

Huang, Jin, Seung-Jin Lee, Saeromi Kang, Man Ho Choi, and Dong-Soon Im. "7α,25-Dihydroxycholesterol Suppresses Hepatocellular Steatosis through GPR183/EBI2 in Mouse and Human Hepatocytes." Journal of Pharmacology and Experimental Therapeutics 374, no. 1 (April 27, 2020): 142–50. http://dx.doi.org/10.1124/jpet.120.264960.

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28

Benned-Jensen, Tau, Christian M. Madsen, Kristine N. Arfelt, Christian Smethurst, Andy Blanchard, Robert Jepras, and Mette M. Rosenkilde. "Small molecule antagonism of oxysterol-induced Epstein-Barr virus induced gene 2 (EBI2) activation." FEBS Open Bio 3, no. 1 (January 1, 2013): 156–60. http://dx.doi.org/10.1016/j.fob.2013.02.003.

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29

Preuss, Inga, Marie-Gabrielle Ludwig, Birgit Baumgarten, Frederic Bassilana, Francois Gessier, Klaus Seuwen, and Andreas W. Sailer. "Transcriptional regulation and functional characterization of the oxysterol/EBI2 system in primary human macrophages." Biochemical and Biophysical Research Communications 446, no. 3 (April 2014): 663–68. http://dx.doi.org/10.1016/j.bbrc.2014.01.069.

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30

Chiang, Eugene Y., Robert J. Johnston, and Jane L. Grogan. "EBI2 Is a Negative Regulator of Type I Interferons in Plasmacytoid and Myeloid Dendritic Cells." PLoS ONE 8, no. 12 (December 26, 2013): e83457. http://dx.doi.org/10.1371/journal.pone.0083457.

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31

Nevius, Erin, Flavia Pinho, Meera Dhodapkar, Huiyan Jin, Kristina Nadrah, Mark C. Horowitz, Junichi Kikuta, Masaru Ishii, and João P. Pereira. "Oxysterols and EBI2 promote osteoclast precursor migration to bone surfaces and regulate bone mass homeostasis." Journal of Cell Biology 211, no. 1 (October 12, 2015): 2111OIA228. http://dx.doi.org/10.1083/jcb.2111oia228.

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32

Gatto, Dominique, Katherine Wood, Irina Caminschi, Danielle Murphy-Durland, Peter Schofield, Daniel Christ, Gunasegaran Karupiah, and Robert Brink. "The chemotactic receptor EBI2 regulates the homeostasis, localization and immunological function of splenic dendritic cells." Nature Immunology 14, no. 5 (March 17, 2013): 446–53. http://dx.doi.org/10.1038/ni.2555.

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33

Clottu, Aurélie S., Amandine Mathias, Andreas W. Sailer, Myriam Schluep, Jörg D. Seebach, Renaud Du Pasquier, and Caroline Pot. "EBI2 Expression and Function: Robust in Memory Lymphocytes and Increased by Natalizumab in Multiple Sclerosis." Cell Reports 18, no. 1 (January 2017): 213–24. http://dx.doi.org/10.1016/j.celrep.2016.12.006.

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34

Deng, Xiaohu, Siquan Sun, Jiejun Wu, Chester Kuei, Victory Joseph, Changlu Liu, and Neelakandha S. Mani. "Fluoro analogs of bioactive oxy-sterols: Synthesis of an EBI2 agonist with enhanced metabolic stability." Bioorganic & Medicinal Chemistry Letters 26, no. 20 (October 2016): 4888–91. http://dx.doi.org/10.1016/j.bmcl.2016.09.029.

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35

Gatto, Dominique, Katherine Wood, Irina Caminschi, Danielle Murphy-Durland, Peter Schofield, Daniel Christ, Gunasegaran Karupiah, and Robert Brink. "Erratum: The chemotactic receptor EBI2 regulates the homeostasis, localization and immunological function of splenic dendritic cells." Nature Immunology 14, no. 8 (July 19, 2013): 876. http://dx.doi.org/10.1038/ni0813-876e.

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36

Misselwitz, Benjamin, Annika Wyss, Tina Raselli, Kirstin Atrott, Isabelle Frey-Wagner, Andreas Sailer, and Gerhard Rogler. "Mo1685 Role of EBI2 and Oxysterols in the Development of Intestinal Lymphoid Structures and Colon Inflammation." Gastroenterology 148, no. 4 (April 2015): S—685. http://dx.doi.org/10.1016/s0016-5085(15)32315-5.

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37

Gatto, Dominique, Didrik Paus, Antony Basten, Charles R. Mackay, and Robert Brink. "Guidance of B Cells by the Orphan G Protein-Coupled Receptor EBI2 Shapes Humoral Immune Responses." Immunity 31, no. 2 (August 2009): 259–69. http://dx.doi.org/10.1016/j.immuni.2009.06.016.

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38

Baptista, Antonio P., Anita Gola, Yuefeng Huang, Pedro Milanez-Almeida, Parizad Torabi-Parizi, Joseph F. Urban, Virginia S. Shapiro, Michael Y. Gerner, and Ronald N. Germain. "The Chemoattractant Receptor Ebi2 Drives Intranodal Naive CD4+ T Cell Peripheralization to Promote Effective Adaptive Immunity." Immunity 50, no. 5 (May 2019): 1188–201. http://dx.doi.org/10.1016/j.immuni.2019.04.001.

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39

Gessier, Francois, Inga Preuss, Hong Yin, Mette M. Rosenkilde, Stephane Laurent, Ralf Endres, Yu A. Chen, et al. "Identification and Characterization of Small Molecule Modulators of the Epstein–Barr Virus-Induced Gene 2 (EBI2) Receptor." Journal of Medicinal Chemistry 57, no. 8 (April 15, 2014): 3358–68. http://dx.doi.org/10.1021/jm4019355.

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40

Thomae, H., R. Becker, H. Bongers, and M. Kleinod. "XEBIST: simplified EBIS/EBIT without magnetic field." Nuclear Instruments and Methods in Physics Research Section B: Beam Interactions with Materials and Atoms 98, no. 1-4 (May 1995): 577–80. http://dx.doi.org/10.1016/0168-583x(95)00015-1.

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41

Kelly, Lisa M., João P. Pereira, Tangsheng Yi, Ying Xu, and Jason G. Cyster. "EBI2 Guides Serial Movements of Activated B Cells and Ligand Activity Is Detectable in Lymphoid and Nonlymphoid Tissues." Journal of Immunology 187, no. 6 (August 15, 2011): 3026–32. http://dx.doi.org/10.4049/jimmunol.1101262.

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42

Niss Arfelt, Kristine, Line Barington, Tau Benned-Jensen, Valentina Kubale, Alexander L. Kovalchuk, Viktorija Daugvilaite, Jan Pravsgaard Christensen, et al. "EBI2 overexpression in mice leads to B1 B-cell expansion and chronic lymphocytic leukemia–like B-cell malignancies." Blood 129, no. 7 (February 16, 2017): 866–78. http://dx.doi.org/10.1182/blood-2016-02-697185.

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43

Wanke, Florian, Sonja Moos, Andrew L. Croxford, André P. Heinen, Stephanie Gräf, Bettina Kalt, Denise Tischner, et al. "EBI2 Is Highly Expressed in Multiple Sclerosis Lesions and Promotes Early CNS Migration of Encephalitogenic CD4 T Cells." Cell Reports 18, no. 5 (January 2017): 1270–84. http://dx.doi.org/10.1016/j.celrep.2017.01.020.

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44

Ki, Sanghee, Hiran M. Thyagarajan, Zicheng Hu, Jessica N. Lancaster, and Lauren I. R. Ehrlich. "EBI2 contributes to the induction of thymic central tolerance in mice by promoting rapid motility of medullary thymocytes." European Journal of Immunology 47, no. 11 (August 9, 2017): 1906–17. http://dx.doi.org/10.1002/eji.201747020.

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45

Sze, Daniel, Tetsuo Yamagishi, Warren Kaplan, Ross D. Brown, Phoebe Joy Ho, John Gibson, and Douglas E. Joshua. "Gene Expression Profiling of the Clinical Significant CD57+CD8+ Cytotoxic T Cell Expansions in Patients with Waldenstrom’s Macroglobulinemia." Blood 108, no. 11 (November 16, 2006): 3395. http://dx.doi.org/10.1182/blood.v108.11.3395.3395.

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Abstract Previous studies have suggested that expanded T-cell clones are found in the blood of 59% of patients with multiple myeloma. These expanded T-cell clones are associated with prolonged overall survival and thus it has been suggested that they may have anti-tumor activity. We have previously reported similar T-cell clones exist in the peripheral blood of patients with Waldenstrom’s Macroglobulinemia (WM) by using flow cytometry to determine the T cell receptor (TCR) Vβ repertoire. Expanded T-cell clones were detected in 9 of 15 (60%) patient samples. Of the nine patients with TCR Vβ clones, four patients had multiple clones. The TCR Vβ clones were not identical, representing a variety of families across the TCR Vβ repertoire. We have previously found that while the TCRVβ+CD8+CD57 negative subset represents polyclonal populations, the CD57 positive subset represents either monoclonal or biclonal populations. By comparing the genetic profiling of these two subsets from a statistically significant gene list, two genes have been found to be highly upregulated in the CD57 negative polyclonal subset. These two genes are i.) SESN3, a member in the Sorting Nexin (SNX) protein family which is implicated in regulating membrane traffic capable of interaction with phosphatidylinositol-3-phosphate (10.4 fold, p=0.0241); ii.) Epstein-Barr virus induced gene 2 (lymphocyte-specific G protein-coupled receptor) EBI2 (7.4 fold, p=0.0207): This finding is in contrast to previous report that EBI2 is expressed in B-lymphocyte cell lines and in lymphoid tissues but not in T-lymphocyte cell lines or peripheral blood T lymphocytes. For the CD57 positive clonal T cell expansions, consistent with our previous reports, CD28 expression was found to be down regulated by 2.6 fold. There are two genes found to be highly upregulated. They are i.) Granzyme B (4.3 fold, p=0.0337) also called Cytotoxic T-lymphocyte proteinase 2. This enzyme is necessary for target cell lysis in cell-mediated immune responses through caspase-dependent apoptosis; ii.) Granzyme H, also called Cytotoxic T-lymphocyte proteinase and probably necessary for target cell lysis in cell-mediated immune responses. In summary, we have shown that CD57 positive clonal T cell populations exist in some patients with WM. Importantly, microarray results have indicated some genes and proteins that may related to better patients survival as previously demonstrated in patients with Multiple Myeloma.

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46

Leeman, Jennifer, Larissa Calancie, Michelle C. Kegler, Cam T. Escoffery, Alison K. Herrmann, Esther Thatcher, Marieke A. Hartman, and Maria E. Fernandez. "Developing Theory to Guide Building Practitioners’ Capacity to Implement Evidence-Based Interventions." Health Education & Behavior 44, no. 1 (July 10, 2016): 59–69. http://dx.doi.org/10.1177/1090198115610572.

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Public health and other community-based practitioners have access to a growing number of evidence-based interventions (EBIs), and yet EBIs continue to be underused. One reason for this underuse is that practitioners often lack the capacity (knowledge, skills, and motivation) to select, adapt, and implement EBIs. Training, technical assistance, and other capacity-building strategies can be effective at increasing EBI adoption and implementation. However, little is known about how to design capacity-building strategies or tailor them to differences in capacity required across varying EBIs and practice contexts. To address this need, we conducted a scoping study of frameworks and theories detailing variations in EBIs or practice contexts and how to tailor capacity-building to address those variations. Using an iterative process, we consolidated constructs and propositions across 24 frameworks and developed a beginning theory to describe salient variations in EBIs (complexity and uncertainty) and practice contexts (decision-making structure, general capacity to innovate, resource and values fit with EBI, and unity vs. polarization of stakeholder support). The theory also includes propositions for tailoring capacity-building strategies to address salient variations. To have wide-reaching and lasting impact, the dissemination of EBIs needs to be coupled with strategies that build practitioners’ capacity to adopt and implement a variety of EBIs across diverse practice contexts.

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47

Cornaby, Caleb, Jillian L. Jafek, Cameron Birrell, Vera Mayhew, Lauren Syndergaard, Jeffrey Mella, Wesley Cheney, and Brian D. Poole. "EBI2 expression in B lymphocytes is controlled by the Epstein–Barr virus transcription factor, BRRF1 (Na), during viral infection." Journal of General Virology 98, no. 3 (March 1, 2017): 435–46. http://dx.doi.org/10.1099/jgv.0.000660.

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48

Zschornack, G., F. Grossmann, U. Kentsch, V. P. Ovsyannikov, E. Ritter, M. Schmidt, A. Thorn, and F. Ullmann. "Status report of the Dresden EBIS/EBIT developments." Review of Scientific Instruments 81, no. 2 (February 2010): 02A512. http://dx.doi.org/10.1063/1.3267846.

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49

Heuck, Christoph J., Saad Zafar Usmani, Erming Tian, Qing Zhang, Frits Van Rhee, Sarah Waheed, Bijay P. Nair, et al. "Marked efficacy of rituximab in two patients with Waldenstrom macroglobulinemia-like multiple myeloma." Journal of Clinical Oncology 30, no. 15_suppl (May 20, 2012): e18548-e18548. http://dx.doi.org/10.1200/jco.2012.30.15_suppl.e18548.

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e18548 Background: Rituximab (R) has been deemed to be ineffective in multiple myeloma (MM), despite CD20 expression in 10-15% of MM. Here we report two cases, selected by a genomic approach, with an excellent response to single agent R. Methods: as below Results: Patient 1: A 49 yr old male with IgG lambda MM with 80% bone marrow (BM) plasma cells (PC) and IgG level of 23 g/L had been treated elsewhere with one cycle of CRD. Here, we noted CD-2 subclass by gene expression profilin (GEP), however without spiked expression of CCND1 and CCND3 genes as manifestation of a t[11:14] or a t[6:14]. GEP further revealed a del 6q and overexpression of EBI2, both commonly seen in Waldenstrom Macroglobulinemia (WM). All findings were confirmed by FISH. Unsupervised clustering in the context of MGUS, untreated MM and WM-PC, confirmed WM-like MM in this patient. Sole therapy with R (750 mg/m2/d x 5d, weekly x 4, bi-weekly x 4 and then monthly) resulted in a reduction of IgG from 1850 mg/dL to 950 mg/dl and BM PC from 60% to 10% at 9 months and a decrease in sLFLC from 68 mg/dL to 10 mg/dL at 12 months follow up. Patient 2: Based on the above observation, we identified a second patient. This 37-yr old male had been diagnosed with lambda light chain MM 42 months earlier with a BM PC of 15%, lambda light-chain proteinuria of 1.9 g/d and sLFLC in the 200mg/dL range. Because of absence of CRAB criteria, he was followed expectantly. Rising BM PC to 50% and concern for end-organ damage motivated a detailed examination of GEP data. GEP showed high expression of CD20 and EBI2 and absence of CCND1 and CCND3 spikes. This was confirmed by FISH, which also revealed a del 6q. As in the first case, this patient co-segregated with WM. R treatment on the same schedule resulted in a reduction of sLFLC levels from 249 mg/dL to 29.9 mg/dl and of Bence Jones proteinuria from 1766 mg/d to 242 mg/d. Conclusions: The presumed lack of activity of R in MM needs to be revisited in light of the marked response noted in these 2 patients. Studies are in progress (a) to extend R therapy to similar cases, and (b) to more fully characterize the prevalence of genetic/phenotypic characteristics, as seen in these 2 cases, among several thousand MM patients. This updated information will be presented at the meeting.

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Klejbor, Ilona, Derya R. Shimshek, Joanna Klimaszewska‐Łata, Maria Velasco‐Estevez, Janusz Moryś, Bartosz Karaszewski, Andrzej Szutowicz, and Aleksandra Rutkowska. "EBI2 is expressed in glial cells in multiple sclerosis lesions, and its knock‐out modulates remyelination in the cuprizone model." European Journal of Neuroscience 54, no. 3 (July 5, 2021): 5173–88. http://dx.doi.org/10.1111/ejn.15359.

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