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1

Shlomchik, Mark J., and Florian Weisel. "Germinal centers." Immunological Reviews 247, no. 1 (2012): 5–10. http://dx.doi.org/10.1111/j.1600-065x.2012.01125.x.

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2

Victora, Gabriel D., and Michel C. Nussenzweig. "Germinal Centers." Annual Review of Immunology 30, no. 1 (2012): 429–57. http://dx.doi.org/10.1146/annurev-immunol-020711-075032.

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3

MacLennan, Ian C. M. "Germinal Centers." Annual Review of Immunology 12, no. 1 (1994): 117–39. http://dx.doi.org/10.1146/annurev.iy.12.040194.001001.

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4

Manser, Tim. "Textbook Germinal Centers?" Journal of Immunology 172, no. 6 (2004): 3369–75. http://dx.doi.org/10.4049/jimmunol.172.6.3369.

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5

Visan, Ioana. "Hypoxic germinal centers." Nature Immunology 17, no. 11 (2016): 1243. http://dx.doi.org/10.1038/ni.3594.

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6

Arakawa, Hiroshi, Kei-ichi Kuma, Masahiro Yasuda, Shuichi Furusawa, Shigeo Ekino, and Hideo Yamagishi. "Oligoclonal Development of B Cells Bearing Discrete Ig Chains in Chicken Single Germinal Centers." Journal of Immunology 160, no. 9 (1998): 4232–41. http://dx.doi.org/10.4049/jimmunol.160.9.4232.

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Abstract Chicken single germinal centers enable us to analyze the postbursal diversifications of B cells due to their easy isolation. Germinal center formation has peaked by day 7 of primary responses and begins to wane 14 days after immunization. To detail the kinetics of Ig mutation and selection, we analyzed Ig light chain sequences recovered from single germinal centers at 7 and 11 days postimmunization with an artificial Ag. Our observations show that multiple, Ag-activated B cells migrating into single germinal centers are diversified by gene conversion in the very early phase of the ger
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7

Toellner, Kai-Michael, William E. Jenkinson, Dale R. Taylor, et al. "Low-level Hypermutation in T Cell–independent Germinal Centers Compared with High Mutation Rates Associated with T Cell–dependent Germinal Centers." Journal of Experimental Medicine 195, no. 3 (2002): 383–89. http://dx.doi.org/10.1084/jem.20011112.

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Exceptionally germinal center formation can be induced without T cell help by polysaccharide-based antigens, but these germinal centers involute by massive B cell apoptosis at the time centrocyte selection starts. This study investigates whether B cells in germinal centers induced by the T cell–independent antigen (4-hydroxy-3-nitrophenyl)acetyl (NP) conjugated to Ficoll undergo hypermutation in their immunoglobulin V region genes. Positive controls are provided by comparing germinal centers at the same stage of development in carrier-primed mice immunized with a T cell–dependent antigen: NP p
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8

de Vinuesa, Carola García, Matthew C. Cook, Jennifer Ball, et al. "Germinal Centers without T Cells." Journal of Experimental Medicine 191, no. 3 (2000): 485–94. http://dx.doi.org/10.1084/jem.191.3.485.

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Germinal centers are critical for affinity maturation of antibody (Ab) responses. This process allows the production of high-efficiency neutralizing Ab that protects against virus infection and bacterial exotoxins. In germinal centers, responding B cells selectively mutate the genes that encode their receptors for antigen. This process can change Ab affinity and specificity. The mutated cells that produce high-affinity Ab are selected to become Ab-forming or memory B cells, whereas cells that have lost affinity or acquired autoreactivity are eliminated. Normally, T cells are critical for germi
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9

He, Yuke, and Carola G. Vinuesa. "Monocytes asphyxiate germinal centers." Immunity 55, no. 3 (2022): 385–87. http://dx.doi.org/10.1016/j.immuni.2022.02.007.

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10

Young, Clara, and Robert Brink. "Germinal centers and autoantibodies." Immunology & Cell Biology 98, no. 6 (2020): 480–89. http://dx.doi.org/10.1111/imcb.12321.

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11

Dempsey, Laurie A. "Dopamine in germinal centers." Nature Immunology 18, no. 9 (2017): 961. http://dx.doi.org/10.1038/ni.3825.

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12

Kroese, Frans G. M., Auk S. Wubbena, Hendrik G. Seijen, and Paul Nieuwenhuis. "Germinal centers develop oligoclonally." European Journal of Immunology 17, no. 7 (1987): 1069–72. http://dx.doi.org/10.1002/eji.1830170726.

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13

Jacob, J., J. Przylepa, C. Miller, and G. Kelsoe. "In situ studies of the primary immune response to (4-hydroxy-3-nitrophenyl)acetyl. III. The kinetics of V region mutation and selection in germinal center B cells." Journal of Experimental Medicine 178, no. 4 (1993): 1293–307. http://dx.doi.org/10.1084/jem.178.4.1293.

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In the murine spleen, germinal centers are the anatomic sites for antigen-driven hypermutation and selection of immunoglobulin (Ig) genes. To detail the kinetics of Ig mutation and selection, 178 VDJ sequences from 16 antigen-induced germinal centers were analyzed. Although germinal centers appeared by day 4, mutation was not observed in germinal center B cells until day 8 postimmunization; thereafter, point mutations favoring asymmetrical transversions accumulated until day 14. During this period, strong phenotypic selection on the mutant B lymphocytes was inferred from progressively biased d
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14

Özkan, Melda Cömert, Nazan Özsan, Mine Hekimgil, Güray Saydam, and Mahmut Töbü. "Progressive Transformation of Germinal Centers: Single Center Experience." Clinical Lymphoma Myeloma and Leukemia 15 (September 2015): S39. http://dx.doi.org/10.1016/j.clml.2015.07.082.

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15

Stengel, Kristy R., Srividya Bhaskara, Jing Wang, et al. "Histone deacetylase 3 controls a transcriptional network required for B cell maturation." Nucleic Acids Research 47, no. 20 (2019): 10612–27. http://dx.doi.org/10.1093/nar/gkz816.

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Abstract Histone deacetylase 3 (Hdac3) is a target of the FDA approved HDAC inhibitors, which are used for the treatment of lymphoid malignancies. Here, we used Cd19-Cre to conditionally delete Hdac3 to define its role in germinal center B cells, which represent the cell of origin for many B cell malignancies. Cd19-Cre-Hdac3−/− mice showed impaired germinal center formation along with a defect in plasmablast production. Analysis of Hdac3−/− germinal centers revealed a reduction in dark zone centroblasts and accumulation of light zone centrocytes. RNA-seq revealed a significant correlation betw
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16

Stoler-Barak, Liat, and Ziv Shulman. "Getting toGether in Germinal centers." Science Immunology 6, no. 60 (2021): eabi9749. http://dx.doi.org/10.1126/sciimmunol.abi9749.

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In this issue of Science Immunology, Gallman et al. reveal how S-geranylgeranyl-l-glutathione cleavage and transport support P2RY8-driven B cell confinement to the germinal centers and its role in lymphocyte homing to the bone marrow.
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17

Domeier, Phillip P., Stephanie L. Schell, and Ziaur S. M. Rahman. "Spontaneous germinal centers and autoimmunity." Autoimmunity 50, no. 1 (2017): 4–18. http://dx.doi.org/10.1080/08916934.2017.1280671.

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18

Verma, Amit, Wendy Stock, Sandhya Norohna, Rajul Shah, Basil Bradlow, and Leonidas C. Platanias. "Progressive Transformation of Germinal Centers." Acta Haematologica 108, no. 1 (2002): 33–38. http://dx.doi.org/10.1159/000063057.

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19

Tarlinton, David. "Germinal centers: form and function." Current Opinion in Immunology 10, no. 3 (1998): 245–51. http://dx.doi.org/10.1016/s0952-7915(98)80161-1.

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20

MacLennan, Ian C. M. "Germinal Centers Still Hold Secrets." Immunity 22, no. 6 (2005): 656–57. http://dx.doi.org/10.1016/j.immuni.2005.06.002.

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21

Moschovakis, G. Leandros, and Reinhold Förster. "Repulsive behavior in germinal centers." Science 356, no. 6339 (2017): 703–4. http://dx.doi.org/10.1126/science.aan5222.

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22

Licup, Ana T., Paolo Campisi, Bo-Yee Ngan, and Vito Forte. "Progressive Transformation of Germinal Centers." Archives of Otolaryngology–Head & Neck Surgery 132, no. 7 (2006): 797. http://dx.doi.org/10.1001/archotol.132.7.797.

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23

Maurer, Daniel P., and Aaron G. Schmidt. "Invasion of the germinal centers." Cell 186, no. 1 (2023): 12–14. http://dx.doi.org/10.1016/j.cell.2022.12.023.

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24

Tan, Lu Ping, Miao Wang, Jan-Lukas Robertus, et al. "miRNA Profiling of B Cell Subsets: Specific miRNA Profile for Germinal Center B Cells with a Marked Variation Between Centroblast and Centrocytes." Blood 112, no. 11 (2008): 1459. http://dx.doi.org/10.1182/blood.v112.11.1459.1459.

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Abstract MiRNAs are a new class of small RNAs, of 19–23 nucleotides that were discovered less than two decades ago. These tiny RNAs can negatively regulate genes at the post-transcriptional level by either triggering translational repression or direct cleavage of mRNAs. It has become evident that miRNAs are involved in hematopoiesis and that the aberrant expression of miRNAs may give rise to hematopoietic malignancies. The aim of our study was to characterize the miRNA profile of naïve, germinal center and memory B cells sorted from tonsils and review expression of selected miRNAs in tonsils
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25

Barrington, Robert, Janet Buhlmann, Xiaogan Wang, Amber Bartlett, Bing Lim, and William Smith. "CD275/ICOSL-independent germinal centers and autoantibody in autoimmune-prone RasGRP1-deficient mice (BA13P.125)." Journal of Immunology 192, no. 1_Supplement (2014): 177.11. http://dx.doi.org/10.4049/jimmunol.192.supp.177.11.

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Abstract Lymphopenia results in favorable microenvironments for the expansion and activation of autoreactive lymphocytes. Mice deficient in guanine nucleotide exchange factor Rasgrp1 (KO) are T lymphopenic early in life and develop a lymphoproliferative disorder with features of human SLE. Our previous work revealed that autoreactive B cells lacking RasGRP1 break tolerance early during development as well as during germinal center responses, suggesting both T cell-independent and -dependent mechanisms are responsible. To understand whether T cells are involved in the breach of tolerance in ger
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26

Agarwal, Anshu, Bishnu P. Nayak, and Kanury V. S. Rao. "B Cell Responses to a Peptide Epitope. VII. Antigen-Dependent Modulation of the Germinal Center Reaction." Journal of Immunology 161, no. 11 (1998): 5832–41. http://dx.doi.org/10.4049/jimmunol.161.11.5832.

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Abstract Germinal center responses to two analogous peptides, PS1CT3 and G32CT3, that differ in sequence only at one position within the B cell epitopic region were examined. In comparison with peptide PS1CT3, peptide G32CT3 elicited a poor germinal center response. By demonstrating equal facility of immune complexes with IgM and IgG Ab isotypes to seed germinal centers, we excluded differences in isotype profiles of early primary anti-PS1CT3 and anti-G32CT3 Ig as the probable cause. Quantitative differences in germinal center responses to the two peptides were also not due to either qualitati
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27

Johansson-Lindbom, Bengt, Sigurdur Ingvarsson, and Carl A. K. Borrebaeck. "Germinal Centers Regulate Human Th2 Development." Journal of Immunology 171, no. 4 (2003): 1657–66. http://dx.doi.org/10.4049/jimmunol.171.4.1657.

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28

Bashyam, Hema. "Germinal centers are free for all." Journal of Experimental Medicine 204, no. 11 (2007): 2497. http://dx.doi.org/10.1084/jem.20411iti2.

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29

Ferry, Judith A., Lawrence R. Zukerberg, and Nancy L. Harris. "Florid Progressive Transformation of Germinal Centers." American Journal of Surgical Pathology 16, no. 3 (1992): 252–58. http://dx.doi.org/10.1097/00000478-199203000-00005.

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30

Degn, Søren E., Cees E. van der Poel, Daniel J. Firl, et al. "Clonal Evolution of Autoreactive Germinal Centers." Cell 170, no. 5 (2017): 913–26. http://dx.doi.org/10.1016/j.cell.2017.07.026.

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31

Imamura, Keiko, Masahiro Yasuda, Brigitte Riwar, Seiji Inui, and Shigeo Ekino. "Characteristic cellular composition of germinal centers." Comparative Immunology, Microbiology and Infectious Diseases 32, no. 5 (2009): 419–28. http://dx.doi.org/10.1016/j.cimid.2007.12.002.

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32

Visan, Ioana. "NF-κB flavors in germinal centers". Nature Immunology 15, № 11 (2014): 1008. http://dx.doi.org/10.1038/ni.3017.

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33

Arulraj, Theinmozhi, Sebastian C. Binder, and Michael Meyer-Hermann. "Antibody Mediated Intercommunication of Germinal Centers." Cells 11, no. 22 (2022): 3680. http://dx.doi.org/10.3390/cells11223680.

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Antibody diversification and selection of B cells occur in dynamic structures called germinal centers (GCs). Passively administered soluble antibodies regulate the GC response by masking the antigen displayed on follicular dendritic cells (FDCs). This suggests that GCs might intercommunicate via naturally produced soluble antibodies, but the role of such GC–GC interactions is unknown. In this study, we performed in silico simulations of interacting GCs and predicted that intense interactions by soluble antibodies limit the magnitude and lifetime of GC responses. With asynchronous GC onset, we
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34

Han, S., K. Hathcock, B. Zheng, T. B. Kepler, R. Hodes, and G. Kelsoe. "Cellular interaction in germinal centers. Roles of CD40 ligand and B7-2 in established germinal centers." Journal of Immunology 155, no. 2 (1995): 556–67. http://dx.doi.org/10.4049/jimmunol.155.2.556.

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Abstract Costimulatory interactions between T and B lymphocytes are crucial for T cell activation and B cell proliferation and differentiation. We have compared the roles of CD40L and B7-2 in the initiation and maturation of humoral immunity by administering anti-CD40 ligand (L) or anti-B7-2 Ab during the early (days -1 to 3) or late (days 6-10) phases of primary responses to thymus-dependent (Td) and -independent (Ti) Ags. Germinal center (GC) formation in response to a Td Ag was inhibited completely by the early administration of anti-CD40L or anti-B7-2 Abs. Later in the response, establishe
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Rajnai, Hajnalka, Ivett Teleki, Gergo Kiszner, et al. "Connexin 43 Communication Channels in Follicular Dendritic Cell Development and in Follicular Lymphomas." Journal of Immunology Research 2015 (2015): 1–10. http://dx.doi.org/10.1155/2015/528098.

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Follicular dendritic cells (FDC) show homo- and heterocellular metabolic coupling through connexin 43 (Cx43) gap junctions and support B cell selection and maturation in germinal centers. In follicular lymphomas B cells escape apoptosis while FDC develop abnormally. Here we tested Cx43 channels in reactive FDC development and follicular lymphomas. In culture, the treatment of FDC-B cell clusters (resembling to “ex vivo” germinal centers) with Gap27 peptide, mimicking the 2nd extracellular loop of Cx43 protein, significantly impaired FDC-B cell cluster formation and cell survival. In untreated
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36

Krenacs, Tibor, and Martin Rosendaal. "Gap-Junction Communication Pathways in Germinal Center Reactions." Developmental Immunology 6, no. 1-2 (1998): 111–18. http://dx.doi.org/10.1155/1998/45913.

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Intercellular channels called gap junctions enable multicellular organisms to exchange information rapidly between cells. Though gap junctions are held to be ubiquitous in solid tissues, we have only recently found them in the lymphoid organs. Functional direct cell-cell communication has now been confirmed by us and other groups in bone marrow, thymus, and in secondary lymphoid tissues. What functions do they serve in the lymphoreticular system where, so far, only cytokines/growth factors and adhesion molecules have been considered as regulators? Here we show evidence for and refer to publish
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37

Oliver, A. M., F. Martin, and J. F. Kearney. "Mouse CD38 is down-regulated on germinal center B cells and mature plasma cells." Journal of Immunology 158, no. 3 (1997): 1108–15. http://dx.doi.org/10.4049/jimmunol.158.3.1108.

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Abstract Germinal center formation is the result of antigenic stimulation of B cells in a T cell-rich area. B cells cycle through the germinal centers, and a small percentage survive to become plasma cells or memory B cells. The transformation from a mature B cell into a germinal center B cell and finally into a terminally differentiated B cell is not well understood. Human CD38 is highly expressed on both germinal center B cells and plasma cells, and is useful in delineating these B cell subsets and in understanding the signaling events involved in the development of these B cells. To determi
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38

Fyfe, G., J. A. Cebra-Thomas, E. Mustain, J. M. Davie, C. D. Alley, and M. H. Nahm. "Subpopulations of B lymphocytes in germinal centers." Journal of Immunology 139, no. 7 (1987): 2187–94. http://dx.doi.org/10.4049/jimmunol.139.7.2187.

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Abstract With two new monoclonal antibodies and flow cytometry, we defined three subpopulations among B cells expressing binding sites for peanut agglutinin (i.e., B cells of the germinal center). On monoclonal antibody (5B5) binds globotriaosyl ceramide. The B lymphocytes binding 5B5 have binding sites for peanut agglutinin on the surface and express only small amounts of sIgD and sIgM. When tested against a panel of B cell lines, only Burkitt's lymphoma cells were 5B5+. Moreover, the 5B5+ cells have larger average sizes and a large fraction of proliferating cells. The other monoclonal antibo
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39

İkincioğulları, Aykut. "Cervical lymphadenopathy: progressive transformation of germinal centers." Turkish Journal of Ear Nose and Throat 23, no. 5 (2013): 307–11. http://dx.doi.org/10.5606/kbbihtisas.2013.79966.

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40

Degn, Søren E., Cees E. van der Poel, and Michael C. Carroll. "Targeting autoreactive germinal centers to curb autoimmunity." Oncotarget 8, no. 53 (2017): 90624–25. http://dx.doi.org/10.18632/oncotarget.21701.

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41

Tas, J. M. J., L. Mesin, G. Pasqual, et al. "Visualizing antibody affinity maturation in germinal centers." Science 351, no. 6277 (2016): 1048–54. http://dx.doi.org/10.1126/science.aad3439.

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42

Thorbecke, G. J., A. R. Amin, and V. K. Tsiagbe. "Biology of germinal centers in lymphoid tissue." FASEB Journal 8, no. 11 (1994): 832–40. http://dx.doi.org/10.1096/fasebj.8.11.8070632.

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43

Kelsoe, Garnett. "Life and Death in Germinal Centers (Redux)." Immunity 4, no. 2 (1996): 107–11. http://dx.doi.org/10.1016/s1074-7613(00)80675-5.

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44

Tarlinton, David. "Germinal centers: A second childhood for lymphocytes." Current Biology 7, no. 3 (1997): R155—R159. http://dx.doi.org/10.1016/s0960-9822(97)70077-0.

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45

Victora, Gabriel D., and Luka Mesin. "Clonal and cellular dynamics in germinal centers." Current Opinion in Immunology 28 (June 2014): 90–96. http://dx.doi.org/10.1016/j.coi.2014.02.010.

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46

Quizon, Nicolas, Kihyuck Kwak, Shivem Shah, Ankur Singh, and Susan Pierce. "Bioengineered organoid models of human germinal centers." Journal of Immunology 200, no. 1_Supplement (2018): 120.14. http://dx.doi.org/10.4049/jimmunol.200.supp.120.14.

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Abstract B cells undergo affinity maturation to T cell-dependent antigens within specialized microenvironments in secondary lymphoid organs termed germinal centers (GCs) resulting in the selective proliferation and differentiation of high-affinity B cells. Selection is driven by the ability of antigen-specific GC B cells to extract antigen presented on follicular dendritic cells and subsequently recruit stimuli from T follicular helper cells. Successful GC B cells ultimately differentiate into plasma cells that secrete large amounts of antigen-specific antibody, or memory B cells that contribu
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47

Niedobitek, G., H. Herbst, LS Young, et al. "Patterns of Epstein-Barr virus infection in non-neoplastic lymphoid tissue." Blood 79, no. 10 (1992): 2520–26. http://dx.doi.org/10.1182/blood.v79.10.2520.2520.

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Abstract Taking advantage of the abundant expression of the small Epstein-Barr virus (EBV)-encoded RNAs (EBERs) in latently infected cells, we have analyzed 72 normal and hyperplastic lymph nodes and three tonsils of acute infectious mononucleosis (IM) for the presence and distribution of EBV+ cells using EBER-specific in situ hybridization, in some cases combined with immunohistologic demonstration of cell type- characteristic antigens. In IM, large numbers of EBV+ lymphoid B blasts were detectable in extrafollicular areas, whereas germinal centers were generally free of EBV+ cells. In reacti
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48

Niedobitek, G., H. Herbst, LS Young, et al. "Patterns of Epstein-Barr virus infection in non-neoplastic lymphoid tissue." Blood 79, no. 10 (1992): 2520–26. http://dx.doi.org/10.1182/blood.v79.10.2520.bloodjournal79102520.

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Taking advantage of the abundant expression of the small Epstein-Barr virus (EBV)-encoded RNAs (EBERs) in latently infected cells, we have analyzed 72 normal and hyperplastic lymph nodes and three tonsils of acute infectious mononucleosis (IM) for the presence and distribution of EBV+ cells using EBER-specific in situ hybridization, in some cases combined with immunohistologic demonstration of cell type- characteristic antigens. In IM, large numbers of EBV+ lymphoid B blasts were detectable in extrafollicular areas, whereas germinal centers were generally free of EBV+ cells. In reactive lymph
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49

McHeyzer-Williams, M. G., M. J. McLean, P. A. Lalor, and G. J. Nossal. "Antigen-driven B cell differentiation in vivo." Journal of Experimental Medicine 178, no. 1 (1993): 295–307. http://dx.doi.org/10.1084/jem.178.1.295.

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The secretion of specific antibodies and the development of somatically mutated memory B cells in germinal centers are consequences of T cell-dependent challenge with the hapten (4-hydroxy-3-nitrophenyl)acetyl (NP). Using six-parameter flow cytometry and single cell molecular analysis we can directly monitor the extent of somatic hypermutation in individual responsive (isotype switched) antigen-specific B cells. The current study provides a direct quantitative assessment of recruitment into the antibody-secreting compartment on the one hand, and the germinal center pathway to memory on the oth
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50

Baeza, Carlos Wong, Albany Resendiz, Carla Landa, et al. "Affinity maturation of anti-lipid IgG antibodies produced via germinal center." Journal of Immunology 198, no. 1_Supplement (2017): 74.14. http://dx.doi.org/10.4049/jimmunol.198.supp.74.14.

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Abstract Non-bilayer phospholipid arrangements (NPA) are lipid associations different to the bilayer and are found on cell membranes; they participate in different cellular functions and are transient, but when they are stabilized by drugs such as chlorpromazine, they become immunogenic and induce the formation of anti-NPA antibodies. Mice that receive stabilized NPA share several characteristics with patients with systemic lupus erythematosus, such as the presence of anti-cardiolipin, anti-histone and anti-nuclear antibodies, lupus band, malar exanthema and glomerulonephritis. Mice with this
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