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Journal articles on the topic 'B-1 B cells'

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Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

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1

Yeo, Seung Geun, Joong Saeng Cho, Dong Choon Park, and Thomas L. Rothstein. "B-1 Cells Differ from Conventional B (B-2) Cells: Difference in Proliferation." Immune Network 4, no. 3 (2004): 155. http://dx.doi.org/10.4110/in.2004.4.3.155.

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2

Montecino-Rodriguez, Encarnacion, and Kenneth Dorshkind. "Formation of B-1 B Cells from Neonatal B-1 Transitional Cells Exhibits NF-κB Redundancy." Journal of Immunology 187, no. 11 (October 26, 2011): 5712–19. http://dx.doi.org/10.4049/jimmunol.1102416.

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3

Popi, Ana Flavia. "B-1 phagocytes: the myeloid face of B-1 cells." Annals of the New York Academy of Sciences 1362, no. 1 (July 6, 2015): 86–97. http://dx.doi.org/10.1111/nyas.12814.

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4

Savitsky, David, and Kathryn Calame. "B-1 B lymphocytes require Blimp-1 for immunoglobulin secretion." Journal of Experimental Medicine 203, no. 10 (September 5, 2006): 2305–14. http://dx.doi.org/10.1084/jem.20060411.

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B-1 B cells produce circulating natural antibodies that provide “innate-like” protection against bacterial and viral pathogens. They also provide adaptive responses to blood and air-borne pathogens. B lymphocyte–induced maturation protein 1 (Blimp-1) is a transcriptional repressor that is required for the formation of B-2–derived antibody-secreting plasma cells. In this study, we used mice lacking Blimp-1 in the B cell lineage to show that Blimp-1 is not necessary for the formation or self-renewal of B-1 B cells but that Blimp-1 is required for normal immunoglobulin (Ig) secretion by B-1 cells. B-1 cells lacking Blimp-1 do not repress Pax5 mRNA and do not induce X-box binding protein 1, and μ secreted mRNA normally, showing that B-1 and B-2 cells both use a common pathway for Ig secretion. Blimp-1–deficient B-1 B cells are also defective in providing early protection against influenza infection.

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5

Quách, Tâm D., Thomas J. Hopkins, Nichol E. Holodick, Raja Vuyyuru, Tim Manser, Ruthee-Lu Bayer, and Thomas L. Rothstein. "Human B-1 and B-2 B Cells Develop from Lin−CD34+CD38loStem Cells." Journal of Immunology 197, no. 10 (October 7, 2016): 3950–58. http://dx.doi.org/10.4049/jimmunol.1600630.

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6

Kantor, Aaron B. "The development and repertoire of B-1 cells (CD5 B cells)." Immunology Today 12, no. 11 (November 1991): 389–91. http://dx.doi.org/10.1016/0167-5699(91)90136-h.

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7

HASTINGS, W., S. GURDAK, J. TUMANG, and T. ROTHSTEIN. "CD5+/Mac-1− peritoneal B cells: A novel B cell subset that exhibits characteristics of B-1 cells." Immunology Letters 105, no. 1 (May 15, 2006): 90–96. http://dx.doi.org/10.1016/j.imlet.2006.01.002.

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8

Rabin, E. M., J. Ohara, and W. E. Paul. "B-cell stimulatory factor 1 activates resting B cells." Proceedings of the National Academy of Sciences 82, no. 9 (May 1, 1985): 2935–39. http://dx.doi.org/10.1073/pnas.82.9.2935.

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9

MURAKAMI, MASAO, and TASUKU HONJO. "B-1 Cells and Autoimmunitya." Annals of the New York Academy of Sciences 764, no. 1 (June 28, 2008): 402–9. http://dx.doi.org/10.1111/j.1749-6632.1995.tb55855.x.

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10

Sindhava, Vishal J., and Subbarao Bondada. "Autoregulatory B-1 cells (34.13)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 34.13. http://dx.doi.org/10.4049/jimmunol.182.supp.34.13.

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Abstract Immunological tolerance in the periphery is mediated by clonal inactivation mechanisms as well as by regulatory cells. Recent studies showed that high IL-10 producing B-cell subsets with varying phenotype can regulate different immune responses in numerous mouse models. We found that, in comparison to B-2 cells, peritoneal B-1a cells are hyporesponsive to TLR stimulation in proliferation and antibody secretion, but produce very high amounts of IL-10. We hypothesized that the high IL-10 levels work in an autocrine manner and autoregulate B-1 cells that are prone to produce autoantibodies. Accordingly, neutralization of IL-10 enhanced peritoneal B-1, but not splenic B-2 cell proliferation and differentiation to all TLRs tested. Moreover, IL-10-/- peritoneal B-1 B-cells responded better than wild type B-1 cells to TLR stimulation. Co-stimulation with CD40 and BAFF, but not IL-5, overcame the inhibitory effect of IL-10. The increased IL-10 production was unique to peritoneal B-1 B-cells, since splenic B-1 B cells behaved like splenic B-2 cells, in terms of IL-10 production and proliferation. This autoregulation appears to have physiological significance since IL-10 knock out peritoneal B-1 cells controlled Borrelia hermsii infection better than wild type B-1 cells. Thus the IL-10 mediated autoregulation of B-1 cells may have a role in the control of autoimmunity and infection. (Supported by NIH grants to SB).

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11

Wen, Lijun, Susan A. Shinton, Richard R. Hardy, and Kyoko Hayakawa. "Association of B-1 B Cells with Follicular Dendritic Cells in Spleen." Journal of Immunology 174, no. 11 (May 19, 2005): 6918–26. http://dx.doi.org/10.4049/jimmunol.174.11.6918.

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12

Rowley, Ben, Lingjuan Tang, Susan Shinton, Kyoko Hayakawa, and Richard R. Hardy. "Autoreactive B-1 B cells: Constraints on natural autoantibody B cell antigen receptors." Journal of Autoimmunity 29, no. 4 (December 2007): 236–45. http://dx.doi.org/10.1016/j.jaut.2007.07.020.

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13

O'garra, Anne, Ray Chang, Ning Go, Robin Hastings, Geoffrey Haughton, and Maureen Howard. "Ly-1 B (B-1) cells are the main source of B cell-derived interleukin 10." European Journal of Immunology 22, no. 3 (March 1992): 711–17. http://dx.doi.org/10.1002/eji.1830220314.

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14

Shimomura, Y., E. Mizoguchi, K. Sugimoto, R. Kibe, Y. Benno, A. Mizoguchi, and A. K. Bhan. "Regulatory role of B-1 B cells in chronic colitis." International Immunology 20, no. 6 (April 1, 2008): 729–37. http://dx.doi.org/10.1093/intimm/dxn031.

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15

Hardy, Richard R. "B-1 B cells: development, selection, natural autoantibody and leukemia." Current Opinion in Immunology 18, no. 5 (October 2006): 547–55. http://dx.doi.org/10.1016/j.coi.2006.07.010.

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16

Raveché, E. S., J. Phillips, F. Mahboudi, A. Dang, H. Fernandes, S. Ramachandra, T. Lin, and B. Peng. "Regulatory aspects of clonally expanded B-1 (CD5+B) cells." International Journal of Clinical & Laboratory Research 22, no. 1-4 (March 1992): 220–34. http://dx.doi.org/10.1007/bf02591428.

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17

Tung, James, Kristine Veys, Daryl Sembrano, Casey Hall, and Christian Ross. "Expression profiling of B-1 and B-2 progenitors (36.15)." Journal of Immunology 184, no. 1_Supplement (April 1, 2010): 36.15. http://dx.doi.org/10.4049/jimmunol.184.supp.36.15.

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Abstract B-1 and B-2 comprise the two B cell lineages. B-1 and B-2 cells can be distinguished by their surface phenotype and also by their developmental ontology, immunoglobulin repertoire, anatomical localization, and immune functions. Importantly, B-1 cells arise early in fetal liver while B-2 cells are generated in the bone marrow after birth. The appearance of B-1 and B-2 cells is the result of fetal B-cell development versus adult B-cell development. B-1 and B-2 cells are generated from distinct progenitor cells, namely B-1 progenitors and B-2 progenitors. B-1 progenitors express CD19 but do not express B220. In contrast, B-2 progenitors express B220 but do not express CD19. To determine the fate decisions that led to fetal versus adult B cell development, we sorted B-1 progenitor cells from fetal liver and B-2 progenitor cells from adult bone marrow and performed gene expression array analysis. In our poster, we will present the results of the expression array comparison between the two progenitor populations. We will confirm the expression array comparison results by molecular techniques and discuss the potential significance of these differences.

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18

Holodick, Nichol E., and Thomas L. Rothstein. "B cells in the aging immune system: time to consider B-1 cells." Annals of the New York Academy of Sciences 1362, no. 1 (July 20, 2015): 176–87. http://dx.doi.org/10.1111/nyas.12825.

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19

Wong, Siew-Cheng, Weng-Keong Chew, Joy En-Lin Tan, Alirio J. Melendez, Florence Francis, and Kong-Peng Lam. "Peritoneal CD5+B-1 Cells Have Signaling Properties Similar to Tolerant B Cells." Journal of Biological Chemistry 277, no. 34 (June 17, 2002): 30707–15. http://dx.doi.org/10.1074/jbc.m202460200.

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20

Kivisäkk, P., GV Alm, WZ Tian, D. Matusevicius, S. Fredrikson, and H. Link. "Neutralising and binding anti-interferon-β-1 b (IFN-b-1 b) antibodies during IFN-β-1 b treatment of multiple sclerosis." Multiple Sclerosis Journal 3, no. 3 (June 1997): 184–90. http://dx.doi.org/10.1177/135245859700300303.

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Interferon-β-1b (IFN-β-1b) is an immunomodulatory therapy of multiple sclerosis (MS), reducing the numbers and severity of exacerbations and the total lesion load measured by magnetic resonance imaging of the brain. The benefits of IFN-β-1b could be hampered by the development of neutralising antibodies against the compound. Our results confirmed earlier studies, showing that 42% of MS patients treated with IFN-β-1b for more than 3 months had developed neutralising antibodies. The occurrence of binding anti-IFN-β-1b antibodies, presently not believed to impede the clinical efficacy of IFN-β-1b, were demonstrated by an immunoassay in some patients already after I month of treatment and in 78% after 3 months. The development of binding antibodies seemed to be an early phenomenon, preceding the appearance of neutralising antibodies. Antibodies crossreacting with IFN-β-1a and natural IFN-β were also found in a majority of IFN-β-1b treated patients with high titres of binding antibodies. Employing a solid-phase enzyme-linked immunospot (ELISPOT) assay, 68% of MS patients treated with IFN-β-1b for 1 -23 months had elevated numbers of anti-IFN-β-1b-antibody secreting cells in blood, compared to 18% of untreated MS patients and 20% among patients with other neurological diseases. Thus, our findings confirm that IFN-β-1 b is immunogenic in MS patients. High levels of anti-IFN-β-1b antibody secreting cells were, however, also found in two untreated control patients with inflammatory diseases, suggesting that anti-IFN-β-1b antibodies might also occur spontaneously.

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21

DeF, A. L. "How do B-1 cells originate?" Nature 357, no. 6373 (May 1992): 14. http://dx.doi.org/10.1038/357014b0.

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22

Su, I.-hsin, and Alexander Tarakhovsky. "B-1 cells: orthodox or conformist?" Current Opinion in Immunology 12, no. 2 (April 2000): 191–94. http://dx.doi.org/10.1016/s0952-7915(99)00071-0.

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23

Dempsey, Laurie A. "CD148 function in B-1 cells." Nature Immunology 18, no. 1 (January 2017): 14. http://dx.doi.org/10.1038/ni.3652.

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24

Arnold, Larry W., Suzanne K. McCray, Calin Tatu, and Stephen H. Clarke. "Identification of a Precursor to Phosphatidyl Choline-Specific B-1 Cells Suggesting That B-1 Cells Differentiate from Splenic Conventional B Cells In Vivo: Cyclosporin A Blocks Differentiation to B-1." Journal of Immunology 164, no. 6 (March 15, 2000): 2924–30. http://dx.doi.org/10.4049/jimmunol.164.6.2924.

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25

YOKOTA, SADAKI, TSUNEYOSHI FUNAI, and ARATA ICHIYAMA. "ORGANELLE LOCALIZATION OF RAT LIVER SERINE:PYRUVATE AMINOTRANSFERASE EXPRESSED IN TRANSFECTED COS-1 CELLS ." Biomedical Research 12, no. 1 (1991): 53–59. http://dx.doi.org/10.2220/biomedres.12.53.

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26

BOBRYSHEV, YURI V., and REGINALD S. A. LORD. "Vascular dendritic cells express intercellular adhesion molecule-1 in atherosclerotic plaques ." Biomedical Research 18, no. 2 (1997): 179–82. http://dx.doi.org/10.2220/biomedres.18.179.

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27

Clarke, Stephen H., and Larry W. Arnold. "B-1 Cell Development: Evidence for an Uncommitted Immunoglobulin (Ig)M+ B Cell Precursor in B-1 Cell Differentiation." Journal of Experimental Medicine 187, no. 8 (April 20, 1998): 1325–34. http://dx.doi.org/10.1084/jem.187.8.1325.

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Murine phosphatidyl choline (PtC)–specific B cells in normal mice belong exclusively to the B-1 subset. Analysis of anti-PtC (VH12 and VH12/Vκ4) transgenic (Tg) mice indicates that exclusion from B-0 (also known as B-2) occurs after immunoglobulin gene rearrangement. This predicts that PtC-specific B-0 cells are generated, but subsequently eliminated by either apoptosis or differentiation to B-1. To investigate the mechanism of exclusion, PtC-specific B cell differentiation was examined in mice expressing the X-linked immunodeficiency (xid) mutation. xid mice lack functional Bruton's tyrosine kinase (Btk), a component of the B cell receptor signal transduction pathway, and are deficient in B-1 cell development. We find in C57BL/ 6.xid mice that VH12 pre-BII cell selection is normal and that PtC-specific B cells undergo modest clonal expansion. However, the majority of splenic PtC-specific B cells in anti-PtC Tg/xid mice are B-0, rather than B-1 as in their non-xid counterparts. These data indicate that PtC-specific B-0 cell generation precedes segregation as predicted, and that Btk function is required for efficient segregation to B-1. Since xid mice exhibit defective B cell differentiation, not programmed cell death, these data are most consistent with an inability of PtC-specific B-0 cells to convert to B-1 and a single B cell lineage.

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28

Elgueta, Raul, Dan Tse, Sophie J. Deharvengt, Marcus R. Luciano, Catherine Carriere, Randolph J. Noelle, and Radu V. Stan. "Endothelial Plasmalemma Vesicle–Associated Protein Regulates the Homeostasis of Splenic Immature B Cells and B-1 B Cells." Journal of Immunology 197, no. 10 (October 14, 2016): 3970–81. http://dx.doi.org/10.4049/jimmunol.1501859.

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29

Yamamoto, Shinji, Yoshihiro Wada, Yoshiharu Ishikawa, and Koichi Kadota. "Precursor B-1 B Cell Lymphoma in a Newborn Calf." Journal of Veterinary Diagnostic Investigation 19, no. 4 (July 2007): 447–50. http://dx.doi.org/10.1177/104063870701900422.

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A newborn Holstein female calf had neoplastic lesions in the skin and within the thoracic and abdominal cavities but not in the bone marrow, spleen, thymus, or most lymph nodes. Because the tumor cells were positive for CD79a (B cell marker), CD5 (B-1 cell marker) and terminal deoxynucleotidyl transferase (marker for immature lymphoid precursors), a diagnosis of precursor B-1 B cell lymphoma was made. The diagnosis was strongly supported by the fact that B-1 cells can develop in the fetus, unlike B-2 cells, which are produced after birth. The lymphoma was distinct from the typical calf form of lymphoma of B-2 cell origin, which does not express CD5 and is characterized by generalized lymphadenopathy and involvement of the bone marrow, blood and spleen.

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30

Rekow, Michaela M., Eric J. Darrah, Wadzanai P. Mboko, Philip T. Lange, and Vera L. Tarakanova. "Gammaherpesvirus targets peritoneal B-1 B cells for long-term latency." Virology 492 (May 2016): 140–44. http://dx.doi.org/10.1016/j.virol.2016.02.022.

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31

Alugupalli, Kishore R., and Rachel M. Gerstein. "Divide and Conquer: Division of Labor by B-1 B Cells." Immunity 23, no. 1 (July 2005): 1–2. http://dx.doi.org/10.1016/j.immuni.2005.07.001.

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32

Arnold, L. W., C. A. Pennell, S. K. McCray, and S. H. Clarke. "Development of B-1 cells: segregation of phosphatidyl choline-specific B cells to the B-1 population occurs after immunoglobulin gene expression." Journal of Experimental Medicine 179, no. 5 (May 1, 1994): 1585–95. http://dx.doi.org/10.1084/jem.179.5.1585.

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Adult mice have two easily recognizable subsets of B cells: the predominant resting population of the spleen, called B-2, and those called B-1, which predominate in coelomic cavities and can express CD5. Some antibody specificities appear to be unique to the B-1 population. Cells expressing antibody specific for phosphatidyl choline (PtC) are the most frequent, comprising 2-10% of peritoneal B cells in normal mice. To understand the basis for the segregation of the anti-PtC specificity to this population, we have produced transgenic (Tg) mice expressing the rearranged VH12 and V kappa 4 genes of a PtC-specific B-1 cell lymphoma. We find that VH12-Tg and VH12/V kappa 4 double-Tg mice develop very high numbers of PtC-specific peritoneal and splenic B cells. These cells have the characteristics of B-1 cells; most are CD5+, and are all IgMhi, B220lo, and CD23-. In the peritoneum these cells are also CD11b+. In addition, adult mice have many splenic B cells (up to one third of Tg+ cells) that express the VH12 Tg but do not bind PtC, presumably because they express a V kappa gene other than V kappa 4. These cells appear to be B-2 cells; they are CD23+, CD11b-, IgMlo, B220hi, and CD5-. Thus, mice given either the VH12 Tg alone or together with the V kappa 4 Tg develop a large population of PtC-specific B cells which belong exclusively to the B-1 population. Since B-2 cells can express the VH12 and V kappa 4 gene separately, we interpret these data to indicate that the events leading to the segregation of PtC-specific B cells to the B-1 population in normal mice are initiated after Ig gene rearrangement and expression. These data are discussed with regard to hypotheses of the origin of B-1 cells. We also find that VH12-Tg mice have a marked decrease in the generation of Tg-expressing B cells in adult bone marrow, but not newborn liver. We speculate that this may be related to positive selection of VH12-expressing B cells during differentiation.

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33

ZHENG, Miao, Shunsuke KIMURA, Junko NIO-KOBAYASHI, and Toshihiko IWANAGA. "The selective distribution of LYVE-1-expressing endothelial cells and reticular cells in the reticulo-endothelial system (RES) ." Biomedical Research 37, no. 3 (2016): 187–98. http://dx.doi.org/10.2220/biomedres.37.187.

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34

Ito, Chie, Hidetoshi Yamazaki, and Toshiyuki Yamane. "Earliest hematopoietic progenitors at embryonic day 9 preferentially generate B-1 B cells rather than follicular B or marginal zone B cells." Biochemical and Biophysical Research Communications 437, no. 2 (July 2013): 307–13. http://dx.doi.org/10.1016/j.bbrc.2013.06.073.

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35

Savage, Hannah P., Vanessa M. Yenson, Sanjam S. Sawhney, Betty J. Mousseau, Frances E. Lund, and Nicole Baumgarth. "Blimp-1–dependent and –independent natural antibody production by B-1 and B-1–derived plasma cells." Journal of Experimental Medicine 214, no. 9 (July 11, 2017): 2777–94. http://dx.doi.org/10.1084/jem.20161122.

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Natural antibodies contribute to tissue homeostasis and protect against infections. They are secreted constitutively without external antigenic stimulation. The differentiation state and regulatory pathways that enable continuous natural antibody production by B-1 cells, the main cellular source in mice, remain incompletely understood. Here we demonstrate that natural IgM-secreting B-1 cells in the spleen and bone marrow are heterogeneous, consisting of (a) terminally differentiated B-1–derived plasma cells expressing the transcriptional regulator of differentiation, Blimp-1, (b) Blimp-1+, and (c) Blimp-1neg phenotypic B-1 cells. Blimp-1neg IgM-secreting B-1 cells are not simply intermediates of cellular differentiation. Instead, they secrete similar amounts of IgM in wild-type and Blimp-1–deficient (PRDM-1ΔEx1A) mice. Blimp-1neg B-1 cells are also a major source of IgG3. Consequently, deletion of Blimp-1 changes neither serum IgG3 levels nor the amount of IgG3 secreted per cell. Thus, the pool of natural antibody-secreting B-1 cells is heterogeneous and contains a distinct subset of cells that do not use Blimp-1 for initiation or maximal antibody secretion.

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36

Kodama, Satoru, Masashi Suzuki, Goro Mogi, Takachika Hiroi, and Hiroshi Kiyono. "ROLES OF NASAL B-1 AND B-2 CELLS IN PROTECTIVE IMMUNITY." Nihon Bika Gakkai Kaishi (Japanese Journal of Rhinology) 39, no. 4 (2000): 329–36. http://dx.doi.org/10.7248/jjrhi1982.39.4_329.

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37

Hayakawa, K., R. R. Hardy, L. A. Herzenberg, and L. A. Herzenberg. "Progenitors for Ly-1 B cells are distinct from progenitors for other B cells." Journal of Experimental Medicine 161, no. 6 (June 1, 1985): 1554–68. http://dx.doi.org/10.1084/jem.161.6.1554.

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Data from previous multiparameter fluorescence-activated cell sorter (FACS) analysis and sorting studies define a subset of murine B cells that expresses the Ly-1 surface determinant in conjunction with IgM, IgD, Ia, and other typical B cell markers. These Ly-1 B cells are physically and functionally distinct. They express more IgM and less IgD than most other B cells; they are not normally found in lymph node or bone marrow; they are always present at low frequencies (1-5%) in normal spleens, and, as we show here, they comprise about half of the B cells (10-20% of total cells) recovered from the peritoneal cavity in normal mice. Furthermore, most of the commonly studied IgM autoantibodies in normal and autoimmune mice are produced by these Ly-1 B cells, even though they seldom produce antibodies to exogenous antigens such as trinitrophenyl-Ficoll or trinitrophenyl-keyhole limpet hemocyanin. Cell transfer studies presented here demonstrate that the progenitors of Ly-1 B cells are different from the progenitors of the predominant B cell populations in spleen and lymph node. In these studies, we used FACS analysis and functional assays to characterize donor-derived (allotype-marked) B cells present in lethally irradiated recipients 1-2 mo after transfer. Surprisingly, adult bone marrow cells typically used to reconstitute B cells in irradiated recipients selectively failed to reconstitute the Ly-1 B subset. Liver, spleen, and bone marrow cells from young mice, in contrast, reconstituted all B cells (including Ly-1 B), and peritoneal "washout" cells (PerC) from adult mice uniquely reconstituted Ly-1 B. Bone marrow did not block Ly-1 B development, since PerC and newborn liver still gave rise to Ly-1 B when jointly transferred with marrow. These findings tentatively assign Ly-1 B to a distinct developmental lineage originating from progenitors that inhabit the same locations as other B cell progenitors in young animals, but move to unique location(s) in adults.

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38

Patzelt, Thomas, Selina J. Keppler, Oliver Gorka, Silvia Thoene, Tim Wartewig, Michael Reth, Irmgard Förster, Roland Lang, Maike Buchner, and Jürgen Ruland. "Foxp1 controls mature B cell survival and the development of follicular and B-1 B cells." Proceedings of the National Academy of Sciences 115, no. 12 (March 5, 2018): 3120–25. http://dx.doi.org/10.1073/pnas.1711335115.

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The transcription factor Foxp1 is critical for early B cell development. Despite frequent deregulation of Foxp1 in B cell lymphoma, the physiological functions of Foxp1 in mature B cells remain unknown. Here, we used conditional gene targeting in the B cell lineage and report that Foxp1 disruption in developing and mature B cells results in reduced numbers and frequencies of follicular and B-1 B cells and in impaired antibody production upon T cell-independent immunization in vivo. Moreover, Foxp1-deficient B cells are impaired in survival even though they exhibit an increased capacity to proliferate. Transcriptional analysis identified defective expression of the prosurvival Bcl-2 family gene Bcl2l1 encoding Bcl-xl in Foxp1-deficient B cells, and we identified Foxp1 binding in the regulatory region of Bcl2l1. Transgenic overexpression of Bcl2 rescued the survival defect in Foxp1-deficient mature B cells in vivo and restored peripheral B cell numbers. Thus, our results identify Foxp1 as a physiological regulator of mature B cell survival mediated in part via the control of Bcl-xl expression and imply that this pathway might contribute to the pathogenic function of aberrant Foxp1 expression in lymphoma.

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39

SAITO, SHUICHI, YUKIO HIRATA, TAIHEI IMAI, FUMIAKI MARUMO, MASAAKI TAKAHASHI, and KAZUHIKO TANZAWA. "THROMBIN AND DEXAMETHASONE UPREGULATE EXPRESSION OF ENDOTHELIN-CONVERTING ENZYME-1 IN RAT ENDOTHELIAL CELLS ." Biomedical Research 18, no. 1 (1997): 81–85. http://dx.doi.org/10.2220/biomedres.18.81.

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40

Li, Wei, Jixin Gao, Xiaoying Ma, Weijie Gu, Ke Zhang, and Yufeng Liu. "Murine B-1 B lymphocytes have active phagocytic and microbicidal abilities (134.31)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 134.31. http://dx.doi.org/10.4049/jimmunol.182.supp.134.31.

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Abstract It has long been recognized that B cells lack phagocytic capabilities. Until recently, B cells from teleost fish were shown to have potent phagocytic abilities for particle antigens; however, whether mammalian B cells are able to accomplish phagocytosis is still not clear. Here we demonstrated that mouse peritoneal cavity (PerC) B-1 B cells, which are thought to be the counterpart of the teleost fish blood B cells, had in vivo and in vitro phagocytic activities to Staphylococcus aureus and polystyrene fluorescent microspheres. Ingestion of particles by B cells led to activation of degradative pathways, resulting in phagolysosome formation and intracellular killing of ingested microbes. About 10% of PerC B cells, mostly CD11b+ B-1 B cells, showed phagocytic activities, and there was no apparent difference between B-1a and B-1b cells in the capabilities for phagocytotisis. Spleen B cells showed a very low degree of phagocytosis. Our results revealed for the first time that mammalian B-1 B cells have phagocytic capacities, which may contribute to their role in innate and adaptive immunity.

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41

Osugui, Lika, Jolanda J. de Roo, Vivian Cristina de Oliveira, Ana Clara Pires Sodré, Frank J. T. Staal, and Ana Flavia Popi. "B-1 cells and B-1 cell precursors prompt different responses to Wnt signaling." PLOS ONE 13, no. 6 (June 21, 2018): e0199332. http://dx.doi.org/10.1371/journal.pone.0199332.

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Lam, Kong-Peng, and Klaus Rajewsky. "B Cell Antigen Receptor Specificity and Surface Density Together Determine B-1 versus B-2 Cell Development." Journal of Experimental Medicine 190, no. 4 (August 16, 1999): 471–78. http://dx.doi.org/10.1084/jem.190.4.471.

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Mice expressing the immunoglobulin (Ig) heavy (H) chain variable (V) region from a rearranged VH12 gene inserted into the IgH locus generate predominantly B-1 cells, whereas expression of two other VH region transgenes (VHB1-8 and VHglD42) leads to the almost exclusive generation of conventional, or B-2, cells. To determine the developmental potential of B cells bearing two distinct B cell antigen receptors (BCRs), one favoring B-1 and the other favoring B-2 cell development, we crossed VH12 insertion mice with mice bearing either VHB1-8 or VHglD42. B cells coexpressing VH12 and one of the other VH genes are readily detected in the double IgH insertion mice, and are of the B-2 phenotype. In mice coexpressing VH12, VHB1-8 and a transgenic κ chain able to pair with both H chains, double H chain–expressing B-2 cells, and B-1 cells that have lost VHB1-8 are generated, whereas VHB1-8 single producers are undetectable. These data suggest that B-1 but not B-2 cells are selected by antigenic stimuli in whose delivery BCR specificity and surface density are of critical importance.

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Ye, Min, Olga Ermakova, and Thomas Graf. "PU.1 is not strictly required for B cell development and its absence induces a B-2 to B-1 cell switch." Journal of Experimental Medicine 202, no. 10 (November 21, 2005): 1411–22. http://dx.doi.org/10.1084/jem.20051089.

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In this paper, we describe the unexpected outgrowth of B lineage cells from PU.1−/− fetal liver cultures. The cells express all early B cell genes tested, including the putative PU.1 target genes IL-7R and EBF but not B220, and can produce immunoglobulin M. However, we observed a delay in the PU.1−/− B cell outgrowth and reduced precursor frequencies, indicating that although PU.1 is not strictly required for B cell commitment, it facilitates B cell development. We also ablated PU.1 in CD19-expressing B lineage cells in vivo, using a Cre-lox approach that allows them to be tracked. PU.1 excision resulted in a shift from B-2 cells to B-1–like cells, which dramatically increased with the age of the mice. Our data indicate that this shift is predominantly caused by a B-2 to B-1 cell reprogramming. Furthermore, we found that B-2 cells express substantially more PU.1 than B-1 cells, which is consistent with the idea that maintenance of the B-2 cell phenotype requires relatively high levels of PU.1, but B-1 cells require little.

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Bhat, Neelima M., Aaron B. Kantor, Marcia M. Bieber, Alan M. Stall, Leonore A. Herzenberg, and Nelson N. H. Teng. "The ontogeny and functional characteristics of human B-1 (CD5+ B) cells." International Immunology 4, no. 2 (1992): 243–52. http://dx.doi.org/10.1093/intimm/4.2.243.

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Hayakawa, K., and R. R. Hardy. "Normal, Autoimmune, and Malignant CD5+ B Cells: The LY-1 B Lineage?" Annual Review of Immunology 6, no. 1 (April 1988): 197–218. http://dx.doi.org/10.1146/annurev.iy.06.040188.001213.

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Hardin, J. A., K. Vos, Y. Kawano, and D. H. Sherr. "A Function for Ly-1+ B Cells." Experimental Biology and Medicine 195, no. 2 (November 1, 1990): 172–82. http://dx.doi.org/10.3181/00379727-195-43129c.

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Herzenberg, Leonore A. "B-1 cells: the lineage question revisited." Immunological Reviews 175, no. 1 (June 2000): 9–22. http://dx.doi.org/10.1111/j.1600-065x.2000.imr017520.x.

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Rothstein, Thomas L., Daniel O. Griffin, Nichol E. Holodick, Tam D. Quach, and Hiroaki Kaku. "Human B-1 cells take the stage." Annals of the New York Academy of Sciences 1285, no. 1 (May 2013): 97–114. http://dx.doi.org/10.1111/nyas.12137.

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Hayakawa, Kyoko, and Richard R. Hardy. "Development and function of B-1 cells." Current Opinion in Immunology 12, no. 3 (June 2000): 346–54. http://dx.doi.org/10.1016/s0952-7915(00)00098-4.

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Barbeiro, Denise Frediani, Hermes Vieira Barbeiro, Joel Faintuch, Suely K. Kubo Ariga, Mario Mariano, Ana Flávia Popi, Heraldo Possolo de Souza, Irineu Tadeu Velasco, and Francisco Garcia Soriano. "B-1 cells temper endotoxemic inflammatory responses." Immunobiology 216, no. 3 (March 2011): 302–8. http://dx.doi.org/10.1016/j.imbio.2010.08.002.

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