Log in

Relevant bibliographies by topics / B-2 B cells / Journal articles

Journal articles on the topic 'B-2 B cells'

To see the other types of publications on this topic, follow the link: B-2 B cells.

Author: Grafiati

Published: 4 June 2021

Last updated: 20 February 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Consult the top 50 journal articles for your research on the topic 'B-2 B cells.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Browse journal articles on a wide variety of disciplines and organise your bibliography correctly.

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

2

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

3

Yeo, Seung Geun, Joong Saeng Cho, and Dong Choon Park. "B Cells in Murine Cervical Lymph Nodes are Conventional B-2 Cells." Journal of Korean Medical Science 21, no. 3 (2006): 391. http://dx.doi.org/10.3346/jkms.2006.21.3.391.

Full text

APA, Harvard, Vancouver, ISO, and other styles

4

Hastings, William D, Joseph R Tumang, Timothy W Behrens, and Thomas L Rothstein. "Peritoneal B-2 cells comprise a distinct B-2 cell population with B-1b-like characteristics." European Journal of Immunology 36, no. 5 (May 2006): 1114–23. http://dx.doi.org/10.1002/eji.200535142.

Full text

APA, Harvard, Vancouver, ISO, and other styles

5

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

6

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.

Full text

APA, Harvard, Vancouver, ISO, and other styles

7

MALENDOWICZ, LUDWIK K., and GASTONE G. NUSSDORFER. "POTENT AND SUSTAINED STIMULATION OF RAT ADRENOCORTICAL CELLS BY 5-BROMO-2'-DEOXYURIDINE ." Biomedical Research 17, no. 3 (1996): 237–39. http://dx.doi.org/10.2220/biomedres.17.237.

Full text

APA, Harvard, Vancouver, ISO, and other styles

8

Pers, Jacques-Olivier, Christophe Jamin, Peter Lydyard, Jeannine Charreire, and Pierre Youinou. "The H2 haplotype regulates the distribution of B cells into B-1a, B-1b and B-2 subsets." Immunogenetics 54, no. 3 (June 1, 2002): 208–11. http://dx.doi.org/10.1007/s00251-002-0457-5.

Full text

APA, Harvard, Vancouver, ISO, and other styles

9

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

10

KANNO, TOMIO, YOSHIAKI HABARA, and YOICHI SATOH. "Ca²⁺ wave propagation in cells of pancreatic acinus reverses after cell dispersion ." Biomedical Research 12, no. 6 (1991): 429–34. http://dx.doi.org/10.2220/biomedres.12.429.

Full text

APA, Harvard, Vancouver, ISO, and other styles

11

Yoshimoto, Hidesuke, and Naomi Ogura. "Effect of Prostaglandin E₂on Human Dental Follicle Cells during Osteogenic Differentiation ." International Journal of Oral-Medical Sciences 16, no. 3-4 (2018): 39–48. http://dx.doi.org/10.5466/ijoms.16.39.

Full text

APA, Harvard, Vancouver, ISO, and other styles

12

Jeannin, Pascale, Yves Delneste, Sybille Lecoanet-Henchoz, Jean-François Gauchat, Jonathan Ellis, and Jean-Yves Bonnefoy. "CD86 (B7-2) on Human B Cells." Journal of Biological Chemistry 272, no. 25 (June 20, 1997): 15613–19. http://dx.doi.org/10.1074/jbc.272.25.15613.

Full text

APA, Harvard, Vancouver, ISO, and other styles

13

TANAKA, Saori, Shigekuni HOSOGI, Yukinori SAWABE, Chikao SHIMAMOTO, Hitoshi MATSUMURA, Toshio INUI, Yoshinori MARUNAKA, and Takashi NAKAHARI. "PPARα induced NOS1 phosphorylation via PI3K/Akt in guinea pig antral mucous cells: NO-enhancement in Ca²⁺-regulated exocytosis ." Biomedical Research 37, no. 3 (2016): 167–78. http://dx.doi.org/10.2220/biomedres.37.167.

Full text

APA, Harvard, Vancouver, ISO, and other styles

14

Jahrsdoerfer, Bernd, Sue E. Blackwell, Thomas Simmet, and George J. Weiner. "Human B Cell Lines and Primary B Cells Actively Secrete Granzyme B in Response to IL-2 Family Cytokines." Blood 110, no. 11 (November 16, 2007): 1340. http://dx.doi.org/10.1182/blood.v110.11.1340.1340.

Full text

Abstract:

Abstract It is widely believed that the main function of B cells is antibody secretion, but not cellular cytotoxicity. Recently we found that human B cells activated with interleukin 21 (IL-21) and antibodies to the B cell receptor (BCR) or immunostimulatory oligonucleotides (CpG ODN) develop a phenotype similar to that of cytotoxic T lymphocytes. B cells treated in such a way start to secrete large amounts of granzyme B (GrB) instead of antibodies and, as in the case of B-chronic lymphocytic leukemia (B-CLL), acquire the capability to induce apoptosis in bystander B-CLL cells in a GrB-dependent manner. Using FACS and ELISpot analyses we could now demonstrate that GrB is actively secreted by B cells in a time-dependent manner and that IL-21 is not the only cytokine that induces GrB in B cells. Also cytokine combinations such as IL-10 and IL-4 as well as IL-10 and IFN-alpha induce GrB in normal B cells and various B cell lines including MEC-1 (CLL), ARH-77 (plasma cell leukemia) and Namalwa (Burkitts lymphoma). We conclude that IL-21 and further cytokines can induce B cells to produce functional granzyme B. Further studies are required to elucidate the interactions with B lymphocytes of cells producing these cytokines such as CD4+ T cells, regulatory T cells, NKT cells and plasmacytoid dendritic cells. Our unexpected findings could have significant implications on our understanding of the role of B cells in immune regulation and for a variety of immune phenomena including auto-, cancer and infectious immunity.

APA, Harvard, Vancouver, ISO, and other styles

15

WESSLEN, NILS, and BO HELLMAN. "THE INFLUX OF Ca²⁺ INTO PANCREATIC β-CELLS AND ITS REGULATION BY GLUCOSE ." Biomedical Research 7, no. 5 (1986): 339–44. http://dx.doi.org/10.2220/biomedres.7.339.

Full text

APA, Harvard, Vancouver, ISO, and other styles

16

Rott, O., J. Charreire, K. Mignon-Godefroy, and E. Cash. "B cell superstimulatory influenza virus activates peritoneal B cells." Journal of Immunology 155, no. 1 (July 1, 1995): 134–42. http://dx.doi.org/10.4049/jimmunol.155.1.134.

Full text

Abstract:

Abstract We evaluated the potential of B cell "superstimulatory" influenza viruses to activate peritoneal B cells (PBC) from BALB/c mice containing both CD5+ and CD5- "sister" cells. Like conventional B cells, PBCs responded to influenza viruses in a hemagglutinin glycoprotein (HA) subtype-specific manner with proliferation and vigorous Ig synthesis. However, a number of HA subtypes that are highly stimulatory for conventional B cells failed to induce significant responses of PBC. Isotype-determination revealed a high predominance of IgM and only very low production of IgA and IgG. HA-activated CD5+ B cells showed a hyperexpression of various activation markers, including MHC class II, intercellular adhesion molecule 1 (CD54), and B7-1 molecules. In contrast to conventional B cells, where activation by HA is antagonized by phorbol esters (PMA), HA and PMA acted synergistically on PBC, suggesting differential activation requirements of B-2 cells vs PBC in response to HA. Like HA stimulation of B-2 cells, virus-triggered proliferation of PBC was abrogated by a simultaneous treatment with F(ab')2 fragments of anti-Ig Ab and exhibited synergistic effects with LPS stimulation. HA-mediated proliferative responses of PBC, but not of B-2 cells, were positively controlled by various cytokines, including IL-4 and IL-10, and to a lesser extent by IL-6. In conclusion, our data present the first example of a stimulation of peritoneal B cells by a polyclonal-activating virus, findings that call for considering infections with polyclonal B cell-stimulatory viruses as a means of expanding the pool of potentially autoreactive CD5+ B cells.

APA, Harvard, Vancouver, ISO, and other styles

17

Nakagawa, T., N. Nakagawa, J. L. Ambrus, and A. S. Fauci. "Differential effects of interleukin 2 vs B cell growth factor on human B cells." Journal of Immunology 140, no. 2 (January 15, 1988): 465–69. http://dx.doi.org/10.4049/jimmunol.140.2.465.

Full text

Abstract:

Abstract The effects of recombinant interleukin 2 (IL-2) and high m.w. (HMW) B cell growth factor (BCGF) were examined on normal human peripheral blood B cells activated with Staphylococcus aureus Cowan I (SAC). When SAC-activated B cells were separated into Tac-antigen (Tac-Ag)+ and Tac-Ag- fractions by a cell sorter, recombinant IL-2 induced only the Tac-Ag+ cells to proliferate, whereas both Tac-Ag+ and Tac-Ag- cells responded to HMW-BCGF (m.w. 60,000). Alternatively, SAC-activated B cells were separated according to density into three fractions: low density (large) cells (82 +/- 15% Tac-Ag+), intermediate density (medium) cells (45 +/- 13% Tac-Ag+), and high density (small) cells (less than 5% Tac-Ag+). Recombinant IL-2 enhanced proliferation of low density cells the most, intermediate density cells less, and high density cells not at all. HMW-BCGF induced all three fractions to proliferate to approximately the same degree. Finally, the effects of IL-2 and BCGF on the DNA and RNA content of the various fractions of B cells was examined. RNA content was greater in IL-2-stimulated B cells than BCGF-stimulated B cells, whereas DNA content was the same in both cell populations. IL-2 and BCGF may preferentially interact with different subpopulations of B cells. The interaction of IL-2 or BCGF with normal activated B cells may induce both similar and different intracellular events.

APA, Harvard, Vancouver, ISO, and other styles

18

Wilson, Stephen M., and Bruce N. Wilkie. "B-1 and B-2 B-cells in the pig cannot be differentiated by expression of CD5." Veterinary Immunology and Immunopathology 115, no. 1-2 (January 2007): 10–16. http://dx.doi.org/10.1016/j.vetimm.2006.10.009.

Full text

APA, Harvard, Vancouver, ISO, and other styles

19

Bueno, C., E. H. J. van Roon, A. Muñoz-López, A. Sanjuan-Pla, M. Juan, A. Navarro, R. W. Stam, and P. Menendez. "Immunophenotypic analysis and quantification of B-1 and B-2 B cells during human fetal hematopoietic development." Leukemia 30, no. 7 (December 29, 2015): 1603–6. http://dx.doi.org/10.1038/leu.2015.362.

Full text

APA, Harvard, Vancouver, ISO, and other styles

20

Jackson, Tanisha A., Christopher L. Haga, Götz R. A. Ehrhardt, Randall S. Davis, and Max D. Cooper. "FcR-Like 2 Inhibition of B Cell Receptor-Mediated Activation of B Cells." Journal of Immunology 185, no. 12 (November 10, 2010): 7405–12. http://dx.doi.org/10.4049/jimmunol.1002305.

Full text

APA, Harvard, Vancouver, ISO, and other styles

21

Meyer, Kerstin B. "B-Myb as a critical regulator of Bcl-2 in human B cells." Immunology 114, no. 1 (January 2005): 23–24. http://dx.doi.org/10.1111/j.1365-2567.2004.02093.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

22

Srikakulapu, Prasad, and Coleen A. McNamara. "B cells and atherosclerosis." American Journal of Physiology-Heart and Circulatory Physiology 312, no. 5 (May 1, 2017): H1060—H1067. http://dx.doi.org/10.1152/ajpheart.00859.2016.

Full text

Abstract:

B cells have emerged as important immune cells in cardiovascular disease. Initial studies have suggested that B cells protect against atherosclerosis development. However, subsequent studies demonstrating aggravation of atherosclerosis by B-2 cells have shed light on the subset-dependent effects of B cells. Here, we review the literature that has led to our current understanding of B cell regulation of atherosclerosis, touching on the importance of subsets, local regulation, human translation, and therapeutic potential.

APA, Harvard, Vancouver, ISO, and other styles

23

HARADA, YOSHITERU, KO HATANAKA, MAKI SAITO, MASATAKA MAJIMA, MICHIKO OGINO, MICHIKO KAWAMURA, TAKASHI OHNO, QIUSHENG YANG, MAKOTO KATORI, and SHOZO YAMAMOTO. "Detection of inducible prostaglandin H synthase-2 in cells in the exudate of rat carrageenin-induced pleurisy ." Biomedical Research 15, no. 2 (1994): 127–30. http://dx.doi.org/10.2220/biomedres.15.127.

Full text

APA, Harvard, Vancouver, ISO, and other styles

24

Irish, Jonathan M., Debra K. Czerwinski, Garry P. Nolan, and Ronald Levy. "Altered B-cell receptor signaling kinetics distinguish human follicular lymphoma B cells from tumor-infiltrating nonmalignant B cells." Blood 108, no. 9 (November 1, 2006): 3135–42. http://dx.doi.org/10.1182/blood-2006-02-003921.

Full text

Abstract:

Abstract The B-cell receptor (BCR) transmits life and death signals throughout B-cell development, and altered BCR signaling may be required for survival of B-lymphoma cells. We used single-cell signaling profiles to compare follicular lymphoma (FL) B cells and nonmalignant host B cells within individual patient biopsies and identified BCR-mediated signaling events specific to lymphoma B cells. Expression of CD20, Bcl-2, and BCR light chain isotype (κ or λ) distinguished FL tumor B-cell and nontumor host B-cell subsets within FL patient biopsies. BCR-mediated signaling via phosphorylation of Btk, Syk, Erk1/2, and p38 occurred more rapidly in tumor B cells from FL samples than in infiltrating nontumor B cells, achieved greater levels of per-cell signaling, and sustained this level of signaling for hours longer than nontumor B cells. The timing and magnitude of BCR-mediated signaling in nontumor B cells within an FL sample instead resembled that observed in mature B cells from the peripheral blood of healthy subjects. BCR signaling pathways that are potentiated specifically in lymphoma cells should provide new targets for therapeutic attention.

APA, Harvard, Vancouver, ISO, and other styles

25

Feldman, Scott, Richard Kasjanski, James E. Norton, Robert C. Kern, David B. Conley, Kevin Welch, Bruce K. Tan, et al. "Reciprocal activation of B cells and group 2 innate lymphoid cells." Journal of Immunology 200, no. 1_Supplement (May 1, 2018): 119.9. http://dx.doi.org/10.4049/jimmunol.200.supp.119.9.

Full text

Abstract:

Abstract B cells can be activated at peripheral sites in chronic inflammatory disease, but the mechanisms that drive this, especially in humans, are unclear. We have reported elevated frequencies of Epstein-Barr virus-induced molecule 2 (EBI2) expressing B cells in tissues from patients with chronic airway inflammation. EBI2 is a marker of extrafollicular plasmablasts, which are activated antibody-secreting cells (ASC). We sought to determine the mechanisms of extrafollicular B cell activation during chronic airway inflammation. ELISpot was used to determine ASC frequency in cells from inflamed nasal tissue or control tonsil tissue. B cells, T cells, and group 2 innate lymphoid cells (ILC2) were isolated from peripheral blood, and B cells were co-cultured with group 2 innate lymphoid cells (ILC2) or T cells. EBI2 expression was assessed by flow cytometry, and gene expression changes were assessed by single cell RNA-seq. Inflamed nasal tissue had a higher frequency of ASC compared to tonsil (p<0.05). The majority of the ASC were contained in the EBI2+ B cell subset in nasal and tonsil tissues. Co-culture of B cells and ILC2 significantly increased the frequency of EBI2+ B cells (p<0.01). B cells co-cultured with ILC2 expressed significantly higher levels of CCL17, CCL22, and FceR2 (>5 fold), compared to freshly isolated B cells, or B cells co-cultured with T cells. ILC2 co-cultured with B cells had significantly increased expression of IL-5, IL-13, and IL-2Ra (>7 fold) compared to freshly isolated ILC2. Our data suggest that not only can ILC2 directly activate B cells, but B cells can also enhance ILC2 function. These findings provide new insights into mechanisms that B cells may play in chronic inflammatory disease.

APA, Harvard, Vancouver, ISO, and other styles

26

Kubo, Makoto, Yoshiko Kamiya, Ryuichi Nagashima, Tatsunori Maekawa, Koji Eshima, Sadahiro Azuma, Etsuro Ohta, and Fumiya Obata. "LRRK2 is expressed in B-2 but not in B-1 B cells, and downregulated by cellular activation." Journal of Neuroimmunology 229, no. 1-2 (December 15, 2010): 123–28. http://dx.doi.org/10.1016/j.jneuroim.2010.07.021.

Full text

APA, Harvard, Vancouver, ISO, and other styles

27

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.

Full text

Abstract:

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).

APA, Harvard, Vancouver, ISO, and other styles

28

Mayer, L. "Terminal maturation of resting B cells by proliferation-independent B cells differentiation factors." Journal of Experimental Medicine 164, no. 2 (August 1, 1986): 383–92. http://dx.doi.org/10.1084/jem.164.2.383.

Full text

Abstract:

Using response to four different BCDF preparations as a model of B cell maturation, we have shown that induction of B cell proliferation abrogates terminal maturation of these cells. In fact, response to some BCDFs can occur in the presence of inhibitors of DNA replication, suggesting that there are proliferation-independent as well as proliferation-dependent BCDFs. These findings cannot be explained by changes in the kinetics of the BCDF response, nor can they be reversed by repletion of media or changing cell densities. Proliferation-independent BCDFs appear to exert their effects on dense, resting 4F2- B cells rather than more activated B cells. This is in contrast to B cell differentiation signals of IL-2 alone or SAC and IL-2 in concert. These data suggest that the current models of B cell activation and maturation may require some reorganization, relegating the proliferative phase of B cell maturation to a lesser role. In addition, evidence is provided for the fact that the resting B cell may have the full complement of receptors for BCDF as well as BCGF and BCPF and may help account for the inherent nonspecificity of the immune response.

APA, Harvard, Vancouver, ISO, and other styles

29

TADA, Hiroyuki, Risako SUZUKI, Eiji NEMOTO, Hidetoshi SHIMAUCHI, Kenji MATSUSHITA, and Haruhiko TAKADA. "Increases in IL-33 production by fimbriae and lipopeptide from Porphyromonas gingivalis in mouse bone marrow-derived dendritic cells via Toll-like receptor 2 ." Biomedical Research 38, no. 3 (2017): 189–95. http://dx.doi.org/10.2220/biomedres.38.189.

Full text

APA, Harvard, Vancouver, ISO, and other styles

30

Muraguchi, A., J. H. Kehrl, D. L. Longo, D. J. Volkman, K. A. Smith, and A. S. Fauci. "Interleukin 2 receptors on human B cells. Implications for the role of interleukin 2 in human B cell function." Journal of Experimental Medicine 161, no. 1 (January 1, 1985): 181–97. http://dx.doi.org/10.1084/jem.161.1.181.

Full text

Abstract:

In the present study, we examined the expression of interleukin 2 (IL-2) receptors on normal human B cells as well as established B cell lines. Anti-Tac monoclonal antibody did not bind to freshly separated normal human B cells. Unexpectedly, with the appropriate activation of the normal B cells by anti-mu antibody, phorbol myristate acetate, or Staphylococcus aureus Cowan I (SAC), Tac antigen was induced on the activated B cells. Anti-Tac antibody showed consistent reactivity with two B cell lines that were infected by human T cell leukemia virus (HTLV) and some reactivity with two out of eight Epstein-Barr virus-transformed B cell lines established from normal adult donors. Immunoprecipitation analysis revealed that antigens of similar size with a molecular weight of 50,000-60,000 can be precipitated with anti-Tac antibody from phytohemagglutinin-stimulated normal T cell blasts and normal activated B cells, as well as a cloned B cell line. Binding assays of IL-2 on normal activated B cells and on the cloned B cell (HS1) revealed that B cells have significantly fewer sites and lower-affinity IL-2 receptors compared with phytohemagglutinin-stimulated normal T cell blasts. Finally, biological properties of the IL-2 receptor on B cells were examined by incubating B cells with recombinant IL-2. It was found that moderate concentrations of IL-2 induce significant enhancement of proliferation and differentiation in SAC-activated normal B cells. These results suggest that normal B cells may express functional IL-2 receptors or closely related proteins and thus IL-2 may play a significant role in the modulation of B cell function.

APA, Harvard, Vancouver, ISO, and other styles

31

Su, Thomas T., Beichu Guo, Bo Wei, Jonathan Braun, and David J. Rawlings. "Signaling in transitional type 2 B cells is critical for peripheral B-cell development." Immunological Reviews 197, no. 1 (February 2004): 161–78. http://dx.doi.org/10.1111/j.0105-2896.2004.0102.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

32

Marcato, Paola, George Mulvey, and Glen D. Armstrong. "Cloned Shiga Toxin 2 B Subunit Induces Apoptosis in Ramos Burkitt's Lymphoma B Cells." Infection and Immunity 70, no. 3 (March 2002): 1279–86. http://dx.doi.org/10.1128/iai.70.3.1279-1286.2002.

Full text

Abstract:

ABSTRACT The Shiga toxins (Stx1 and Stx2), produced by Shigella dysenteriae type 1 and enterohemorrhagic Escherichia coli, consist of one A subunit and five B subunits. The Stx1 and Stx2 B subunits form a pentameric structure that binds to globotriaosylceramide (Gb3-Cer) receptors on eukaryotic cells and promotes endocytosis. The A subunit then inhibits protein biosynthesis, which triggers apoptosis in the affected cell. In addition to its Gb3-Cer binding activity, the data in the following report demonstrate that the Stx2 B pentamer induces apoptosis in Ramos Burkitt's lymphoma B cells independently of A subunit activity. Apoptosis was not observed in A subunit-free preparations of the Stx1 B pentamer which competitively inhibited Stx2 B pentamer-mediated apoptosis. The pancaspase inhibitor, Z-VAD-fmk, prevented apoptosis in Ramos cells exposed to the Stx2 B subunit, Stx1 or Stx2. Brefeldin A, an inhibitor of the Golgi transport system, also prevented Stx2 B subunit-mediated apoptosis. These observations suggest that the Stx2 B subunit must be internalized, via Gb3-Cer receptors, to induce Ramos cell apoptosis. Moreover, unlike the two holotoxins, Stx2 B subunit-mediated apoptosis does not involve inhibition of protein biosynthesis. This study provides further insight into the pathogenic potential of this family of potent bacterial exotoxins.

APA, Harvard, Vancouver, ISO, and other styles

33

Marcato, Paola, George Mulvey, and Glen D. Armstrong. "Cloned Shiga Toxin 2 B Subunit Induces Apoptosis in Ramos Burkitt's Lymphoma B Cells." Infection and Immunity 71, no. 8 (August 2003): 4828. http://dx.doi.org/10.1128/iai.71.8.4828.2003.

Full text

APA, Harvard, Vancouver, ISO, and other styles

34

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

35

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

36

Crow, M. K., J. A. Jover, and S. M. Friedman. "Direct T helper-B cell interactions induce an early B cell activation antigen." Journal of Experimental Medicine 164, no. 5 (November 1, 1986): 1760–72. http://dx.doi.org/10.1084/jem.164.5.1760.

Full text

Abstract:

We have explored the consequences for the B cell of cognate interaction with T cells. Early expression of the B cell-restricted cell surface activation antigen, BLAST-2, has been used as an assay system to measure direct T-B cell collaboration. BLAST-2 is preferentially expressed by allogenic B cells cultured with MHC class II antigen-restricted Th clone cells matched to the DR specificity of the target B cells. B cells cultured with DR-mismatched allospecific Th cells express minimal BLAST-2. Th cell-induced BLAST-2 expression appears to be accessory cell independent and occurs as early as 8 h after initiation of culture, with peak expression at 18 h. Direct T-B cell contact, rather than Th-derived lymphokines, provides the most efficient stimulus for BLAST-2 expression. Crosslinking of sIg on B cells is a poor stimulus for BLAST-2 expression. The BLAST-2 assay permits the evaluation of early events associated with B cell activation through cognate interactions, and may facilitate subsequent studies of the mechanism of B cell differentiation.

APA, Harvard, Vancouver, ISO, and other styles

37

SUZAKI, AI, KEN YAMAGUCHI, MASATOSHI KUSUHARA, NAOKO KAJIMURA, ISAMU ADACHI, and SATOSHI KIMURA. "GASTRIN-RELEASING PEPTIDE INCREASES INTRACELLULAR Ca²⁺ CONCENTRATION AND STIMULATES CELL PROLIFERATION OF VASCULAR SMOOTH MUSCLE CELLS ." Biomedical Research 15, no. 5 (1994): 311–15. http://dx.doi.org/10.2220/biomedres.15.311.

Full text

APA, Harvard, Vancouver, ISO, and other styles

38

Diehl, Cody J., Grant D. Barish, Michael Downes, Meng-Yun Chou, Sven Heinz, Christopher K. Glass, Ronald M. Evans, and Joseph L. Witztum. "Research Resource: Comparative Nuclear Receptor Atlas: Basal and Activated Peritoneal B-1 and B-2 Cells." Molecular Endocrinology 25, no. 3 (March 1, 2011): 529–45. http://dx.doi.org/10.1210/me.2010-0384.

Full text

Abstract:

Abstract Naïve murine B cells are typically divided into three subsets based on functional and phenotypic characteristics: innate-like B-1 and marginal zone B cells vs. adaptive B-2 cells, also known as follicular or conventional B cells. B-1 cells, the innate-immune-like component of the B cell lineage are the primary source of natural antibodies and have been shown to modulate autoimmune diseases, human B-cell leukemias, and inflammatory disorders such as atherosclerosis. On the other hand, B-2 cells are the principal mediators of the adaptive humoral immune response and represent an important pharmacological target for various conditions including rheumatoid arthritis, lupus erythematosus, and lymphomas. Using the resources of the Nuclear Receptor Signaling Atlas program, we used quantitative real-time PCR to assess the complement of the 49 murine nuclear receptor superfamily expressed in quiescent and toll-like receptor (TLR)-stimulated peritoneal B-1 and B-2 cells. We report the expression of 24 nuclear receptors in basal B-1 cells and 25 nuclear receptors in basal B-2 cells, with, in some cases, dramatic changes in response to TLR 4 or TLR 2/1 stimulation. Comparative nuclear receptor profiling between B-1 and peritoneal B-2 cells reveals a highly concordant expression pattern, albeit at quantitatively dissimilar levels. We also found that splenic B cells express 23 nuclear receptors. This catalog of nuclear receptor expression in B-1 and B-2 cells provides data to be used to better understand the specific roles of nuclear receptors in B cell function, chronic inflammation, and autoimmune disease.

APA, Harvard, Vancouver, ISO, and other styles

39

Kline, Gregory H., Tracy A. Hayden, and Norman R. Klinman. "B Cell Maintenance in Aged Mice Reflects Both Increased B Cell Longevity and Decreased B Cell Generation." Journal of Immunology 162, no. 6 (March 15, 1999): 3342–49. http://dx.doi.org/10.4049/jimmunol.162.6.3342.

Full text

Abstract:

Abstract In aged mice the population of mature peripheral B cells is maintained despite a severalfold decrease in the population of bone marrow B cell progenitors. The analysis of the rate of accumulation of 5′-bromo-2-deoxyuridine (BrdU)-labeled splenic B cells in mice fed BrdU for 8 days to 8 wk demonstrated a severalfold increase in the half-life of mature B cells in aged mice. Consistent with a role for decreased B cell turnover in maintaining the mature B cell population of aged mice, several findings indicate that fewer newly generated B cells enter the spleen from the bone marrow in aged vs young adult mice. These include 1) a fourfold decrease in the population of relatively immature splenic B cells, defined as cells that express high levels of heat-stable Ag and accumulate BrdU within 8 wk of labeling; and 2) an equivalent decrease in the population of bone marrow cells representative of later stages of B cell maturation (sIgD−sIgMint-high). Surprisingly, despite a four- to sixfold decrease in pre-B cells, the population of least mature bone marrow B cells (IgD−sIgMvery low) remains intact. Because this population accumulates BrdU-labeled cells more slowly in aged mice than in younger mice, and bone marrow B cells at more mature developmental stages are diminished, it appears that in aged mice B cell development beyond the sIgMvery low stage may be retarded and that cells, therefore, accumulate within this population.

APA, Harvard, Vancouver, ISO, and other styles

40

Humbert, P. O., and L. M. Corcoran. "oct-2 gene disruption eliminates the peritoneal B-1 lymphocyte lineage and attenuates B-2 cell maturation and function." Journal of Immunology 159, no. 11 (December 1, 1997): 5273–84. http://dx.doi.org/10.4049/jimmunol.159.11.5273.

Full text

Abstract:

Abstract Targeted mutation of the gene for the Oct-2 transcription factor in mice caused neonatal lethality and abrogated mitogen-induced proliferation and differentiation of mature B lymphocytes in vitro. Here we show that Oct-2 is required for normal humoral responses upon immunization with T cell-dependent as well as T-independent Ags. oct-2-null T cell behavior was normal, implying a B cell-restricted lesion. oct-2-/- B cells displayed aberrant behavior during activation in vitro: both acquisition of markers of cellular activation and cell survival were diminished. Production of early B lineage cells in the bone marrow was normal, yet mature B cells were under-represented in blood and lymphoid organs. Furthermore, peritoneal B-1 lymphocytes were not detected in animals with a reconstituted oct-2-/- lymphoid system. We conclude that Oct-2 is required for B-1 cell maintenance and for normal Ag-driven maturation of conventional B cells in vivo.

APA, Harvard, Vancouver, ISO, and other styles

41

Minami, M., H. Kawasaki, S. Taira, and H. Nariuchi. "Alloantigen presentation by B cells: two types of alloreactive T cell hybridomas, B cell-reactive and B cell-nonreactive." Journal of Immunology 135, no. 1 (July 1, 1985): 111–16. http://dx.doi.org/10.4049/jimmunol.135.1.111.

Full text

Abstract:

Abstract T cell-depleted, Sephadex G-10-passed unstimulated splenic B cells from C57BL/6 mice stimulated splenic T cells from CKB mice to produce IL 2 and to proliferate. The stimulatory ability of the unstimulated B cells was eliminated by 4000 rad irradiation of the unstimulated stimulator B cells. LPS-activated B cells could stimulate responder T cells more efficiently than unstimulated B cells. For further analysis of allostimulation by B cells, we established a series of alloreactive T cell hybridomas. Forty-five percent of these alloreactive T cell hybridomas could be stimulated to produce IL 2 by either macrophage-dendritic cells or unstimulated B cells. Fifty-five percent of these alloreactive T cell hybridomas could be stimulated by macrophage-dendritic cells but not by unstimulated B cells. T cell hybridomas that were not reactive with unstimulated B cells were also nonreactive to LPS-activated B cells. Analysis of two representative I-Ab-reactive T cell hybridoma clones, B cell-reactive clone CB-11.4 and B cell-nonreactive clone HTB-9.3, revealed again that the stimulatory ability of unstimulated B cells was sensitive to 4000 rad irradiation in the activation of CB-11.4 clone and that CB-11.4 could be stimulated more efficiently by LPS-activated B cells than by unstimulated B cells, but HTB-9.3 could not be stimulated by LPS-activated B cells. Thus, there may be two distinct types of T cells in the alloreaction: B-cell-reactive and B cell-nonreactive.

APA, Harvard, Vancouver, ISO, and other styles

42

Jensen, Christina T., Shabnam Kharazi, Charlotta Böiers, Min Cheng, Anna Lübking, Ewa Sitnicka, and Sten Eirik W. Jacobsen. "FLT3 ligand and not TSLP is the key regulator of IL-7–independent B-1 and B-2 B lymphopoiesis." Blood 112, no. 6 (September 15, 2008): 2297–304. http://dx.doi.org/10.1182/blood-2008-04-150508.

Full text

Abstract:

Abstract Phenotypically and functionally distinct progenitors and developmental pathways have been proposed to exist for fetally derived B-1 and conventional B-2 cells. Although IL-7 appears to be the primary cytokine regulator of fetal and adult B lymphopoiesis in mice, considerable fetal B lymphopoiesis and postnatal B cells are sustained in the absence of IL-7; in humans, B-cell generation is suggested to be largely IL-7–independent, as severe combined immune-deficient patients with IL-7 deficiency appear to have normal B-cell numbers. However, the role of other cytokines in IL-7–independent B lymphopoiesis remains to be established. Although thymic stromal lymphopoietin (TSLP) has been proposed to be the main factor driving IL-7–independent B lymphopoiesis and to distinguish fetal from adult B-cell progenitor development in mice, recent studies failed to support a primary role of TSLP in IL-7–independent fetal B-cell development. However, the role of TSLP in IL-7–independent adult B lymphopoiesis and in particular in regulation of B-1 cells remains to be established. Here we demonstrate that, rather than TSLP, IL-7 and FLT3 ligand are combined responsible for all B-cell generation in mice, including recently identified B-1–specified cell progenitors. Thus, the same IL-7– and FLT3 ligand–mediated signal-ing regulates alternative pathways of fetal and adult B-1 and B-2 lymphopoiesis.

APA, Harvard, Vancouver, ISO, and other styles

43

Fischer, Gavin M., Laura A. Solt, William D. Hastings, Kejian Yang, Rachel M. Gerstein, Barbara S. Nikolajczyk, Stephen H. Clarke, and Thomas L. Rothstein. "Splenic and Peritoneal B-1 Cells Differ in Terms of Transcriptional and Proliferative Features That Separate Peritoneal B-1 from Splenic B-2 Cells." Cellular Immunology 213, no. 1 (October 2001): 62–71. http://dx.doi.org/10.1006/cimm.2001.1860.

Full text

APA, Harvard, Vancouver, ISO, and other styles

44

Bukhari, Ameera M. "IgM+IgD− B cells in Human GALT Harbor Characteristics of B1 B cells." Journal of Immunology 204, no. 1_Supplement (May 1, 2020): 158.14. http://dx.doi.org/10.4049/jimmunol.204.supp.158.14.

Full text

Abstract:

Abstract During embryogenesis, B cell lymphopoiesis occurs in fetal liver (FL) and bone marrow (BM). B cells derived from these organs differ in their Ig VH gene usage, their morphological and functional characteristics, and they home to different organs in the mature fetus. Although in mice, FL-B cells are known to home to the peritoneum and GALT, little is known of these cells in humans. We identified a FL-like B cell population representing 10–20% of total B cells in human GALT (appendix and tonsil), but only 1–2% in peripheral blood. These cells express IgM, but not IgD on their surface, spontaneously secrete antibodies in culture, and preferentially class-switch to IgA upon LPS stimulation, three characteristics of FL-B cells. The GALT IgM+IgD− B cells are negative for immature B cell markers CD10 and CD5, plasma cell markers CD38hi and CD138, the activation marker CD43 and the transitional B cell marker CD24hi as expected for FL B cells. In infants and children less than 10 years of age, most (70%) of these IgM+IgD− cells are CD27- non-memory B cells. These data support the hypothesis that the GALT IgM+IgD− B cells are of FL origin. Consistent with this idea, approximately 50% of the B cells in an appendix from a 1-day-old neonate were IgM+IgD−. Deep BCR sequence analysis of these cells will establish their developmental origin.

APA, Harvard, Vancouver, ISO, and other styles

45

Ghosn, E. E. B., P. Sadate-Ngatchou, Y. Yang, L. A. Herzenberg, and L. A. Herzenberg. "Distinct progenitors for B-1 and B-2 cells are present in adult mouse spleen." Proceedings of the National Academy of Sciences 108, no. 7 (January 31, 2011): 2879–84. http://dx.doi.org/10.1073/pnas.1019764108.

Full text

APA, Harvard, Vancouver, ISO, and other styles

46

Suzuki, Keiichiro, Mikako Maruya, Shimpei Kawamoto, and Sidonia Fagarasan. "Roles of B-1 and B-2 cells in innate and acquired IgA-mediated immunity." Immunological Reviews 237, no. 1 (August 19, 2010): 180–90. http://dx.doi.org/10.1111/j.1600-065x.2010.00941.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

47

Franz, Annette, Annette Bryant, and John Farrant. "Staphylococcal enterotoxin B up-regulates interleukin-2 receptor β chain expression on tonsillar B cells." European Journal of Immunology 23, no. 10 (October 1993): 2696–99. http://dx.doi.org/10.1002/eji.1830231047.

Full text

APA, Harvard, Vancouver, ISO, and other styles

48

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.

Full text

Abstract:

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.

APA, Harvard, Vancouver, ISO, and other styles

49

Arikawa, Kazumune, Fengzhu Zhang, Chieko Taguchi, and Ujjal K. Bhawal. "Circadian Expression of Differentiated Embryonic Chondrocytes Expressed Genes 1 and 2 in Human Oral Squamous Cell Carcinoma HSC-3 Cells ." International Journal of Oral-Medical Sciences 17, no. 1 (June 25, 2018): 33–37. http://dx.doi.org/10.5466/ijoms.17.33.

Full text

APA, Harvard, Vancouver, ISO, and other styles

50

Tornberg, U. C., and D. Holmberg. "B-1a, B-1b and B-2 B cells display unique VHDJH repertoires formed at different stages of ontogeny and under different selection pressures." EMBO Journal 14, no. 8 (April 1995): 1680–89. http://dx.doi.org/10.1002/j.1460-2075.1995.tb07157.x.

Full text

APA, Harvard, Vancouver, ISO, and other styles

We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!