Relevant bibliographies by topics / B-2 B cells

Academic literature on the topic '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:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources 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.

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

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
More sources

Dissertations / Theses on the topic "B-2 B cells"

1

Philips, Julia Rachel. "B-1 and B-2 B cell responses to lipopolysaccharide: Putative roles in the pathogenesis of periodontitis." Thesis, The University of Sydney, 2003. http://hdl.handle.net/2123/1852.

Full text
Abstract:
Periodontal disease is one of the most widespread diseases in humans and is characterised by chronic gingival inflammation and B cell accumulation and resorption of the crest of alveolar bone with subsequent loss of teeth. Porphyromonas gingivalis has been identified as a putative aetiological agent for periodontitis. The aim of the research presented in this thesis was to investigate, using in vitro systems, the responses of autoreactive B-1 and B-2 cells to enterobacterial and nonenterobacterial lipopolysaccharide (LPS) to shed light on the pathogenesis of chronic periodontitis and other diseases involving B cell accumulation and autoantibody production. The hypotheses tested were: (1) B cells respond differently to enterobacterial and non-enterobacterial LPS. (2) B-1 cells are activated by a lower concentration of LPS than B-2 cells. (3) LPS stimulation results in preferential accumulation of B-1 cells. Findings consistent with these hypotheses would provide new evidence for different roles for B-1 and B-2 cells in immune responses and that LPS stimulation could lead to B-1 cell accumulation in diseases thus characterised. Initial experiments investigated the responses of representative B-1 (CH12) and B-2 (WEHI-279) cell lines to preparations of P. gingivalis and Salmonella enteritidis LPS utilising flow cytometric and quantitative molecular methods. The cell lines responded differently to the two LPS preparations. There were significant but limited effects on viability and proliferation in the WEHI-279 cell line, but no significant changes in mRNA expression levels for genes including Toll-like receptors (TLR2, TLR4, RP105), immunoglobulin (IgM), cytokines (IL-6, IL-10), co-stimulatory molecules (CD80, CD86), and regulators of apoptosis (Bcl-2, Bax). In the CH12 cell line however, LPS stimulation had greater effect. Addition of S. enteritidis LPS from a threshold level of 100ng/mL was found to rescue the cells from death, reflected by the percentage viability and proliferation. Stimulation of CH12 cells with S. enteritidis LPS also led to a decrease in expression of RP105 mRNA, which may be part of a negative feedback loop. Interestingly, stimulation with low concentrations P. gingivalis LPS appeared to inhibit proliferation but high LPS concentrations stimulated proliferation of CH12 cells, although no further significant effects were noted in other analyses. Evidence was found that CH12 cells have a high basal level of activation. This suggests that this line is constitutively activated. Stimulation with P. gingivalis or S. enteritidis LPS did not affect the level of CD80 mRNA expression. It is possible that the CH12 line constitutively expresses a maximal level of CD80 (and possibly CD86) and further stimulation will not cause any increase. Since S. enteritidis LPS appeared to have more pronounced effects on both B cell populations, this LPS was used to further investigate B cell subset responses in a mixed splenocyte culture system. Experiments examining percentage viability and number of viable cells indicated that B-1 and B-2 B cells responded differently to LPS stimulation. A threshold level for B-2 cell response (significant increase in cell number) was found to be 100ng/mL LPS, in contrast to the B-1 B cell subset which were only significantly different to the unstimulated cells when stimulated with 50μg/mL LPS. By examining the expression of CD80, the majority of murine splenic B-1 cells were found to activated prior to any LPS stimulation in vitro. In contrast, the B-2 subset showed significant increase in CD80 expression only at high (≥10μg/mL) LPS concentrations. Studies of the division index of B-1 and B-2 cells showed a significant response in both subsets following stimulation with 1μg/mL and 10μg/mL LPS. However, overall, the results are inconsistent with LPS driving the preferential accumulation of B-1 cells in disease states. These experiments provided useful evidence that supported the idea that B-1 and B-2 cells respond differently to LPS. However, these studies were unable to directly address the role of P. gingivalis LPS in periodontitis. It may be that P. gingivalis LPS could have different effects to S. enteritidis LPS on primary B cells. It is still possible that B-1 cells may be more sensitive to P. gingivalis, as opposed to S. enteritidis LPS. Studies by other groups have suggested that the TH1/TH2 profile is skewed towards TH2 in chronic periodontitis and that P. gingivalis may drive this shift via its ability to signal through TLR2 (and modulate TLR4 signalling). Further, recent studies in our laboratories have found that P. gingivalis gingipains are able to polyclonally activate B cells and to break down both IFNγ and IL-12. Future studies should further examine the effects of B-1 and B-2 interactions in the mixed lymphocyte system together with subsequent studies utilising human periodontitis biopsies. The results presented in this thesis, together with work undertaken by other investigators, suggests that LPS could perturb the normal homeostatic mechanisms of the B-1 B cell-subset and increase polyclonal activation therefore contributing to the genesis of pathologies such as chronic periodontitis.
APA, Harvard, Vancouver, ISO, and other styles
2

Philips, Julia Rachel. "B-1 And B-2 B Cell Responses To Lipopolysaccharide: Putative Roles In The Pathogenesis Of Periodontitis." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/4395.

Full text
Abstract:
Master of Science
Periodontal disease is one of the most widespread diseases in humans and is characterised by chronic gingival inflammation and B cell accumulation and resorption of the crest of alveolar bone with subsequent loss of teeth. Porphyromonas gingivalis has been identified as a putative aetiological agent for periodontitis. The aim of the research presented in this thesis was to investigate, using in vitro systems, the responses of autoreactive B-1 and B-2 cells to enterobacterial and nonenterobacterial lipopolysaccharide (LPS) to shed light on the pathogenesis of chronic periodontitis and other diseases involving B cell accumulation and autoantibody production. The hypotheses tested were: (1) B cells respond differently to enterobacterial and non-enterobacterial LPS. (2) B-1 cells are activated by a lower concentration of LPS than B-2 cells. (3) LPS stimulation results in preferential accumulation of B-1 cells. Findings consistent with these hypotheses would provide new evidence for different roles for B-1 and B-2 cells in immune responses and that LPS stimulation could lead to B-1 cell accumulation in diseases thus characterised. Initial experiments investigated the responses of representative B-1 (CH12) and B-2 (WEHI-279) cell lines to preparations of P. gingivalis and Salmonella enteritidis LPS utilising flow cytometric and quantitative molecular methods. The cell lines responded differently to the two LPS preparations. There were significant but limited effects on viability and proliferation in the WEHI-279 cell line, but no significant changes in mRNA expression levels for genes including Toll-like receptors (TLR2, TLR4, RP105), immunoglobulin (IgM), cytokines (IL-6, IL-10), co-stimulatory molecules (CD80, CD86), and regulators of apoptosis (Bcl-2, Bax). In the CH12 cell line however, LPS stimulation had greater effect. Addition of S. enteritidis LPS from a threshold level of 100ng/mL was found to rescue the cells from death, reflected by the percentage viability and proliferation. Stimulation of CH12 cells with S. enteritidis LPS also led to a decrease in expression of RP105 mRNA, which may be part of a negative feedback loop. Interestingly, stimulation with low concentrations P. gingivalis LPS appeared to inhibit proliferation but high LPS concentrations stimulated proliferation of CH12 cells, although no further significant effects were noted in other analyses. Evidence was found that CH12 cells have a high basal level of activation. This suggests that this line is constitutively activated. Stimulation with P. gingivalis or S. enteritidis LPS did not affect the level of CD80 mRNA expression. It is possible that the CH12 line constitutively expresses a maximal level of CD80 (and possibly CD86) and further stimulation will not cause any increase. Since S. enteritidis LPS appeared to have more pronounced effects on both B cell populations, this LPS was used to further investigate B cell subset responses in a mixed splenocyte culture system. Experiments examining percentage viability and number of viable cells indicated that B-1 and B-2 B cells responded differently to LPS stimulation. A threshold level for B-2 cell response (significant increase in cell number) was found to be 100ng/mL LPS, in contrast to the B-1 B cell subset which were only significantly different to the unstimulated cells when stimulated with 50μg/mL LPS. By examining the expression of CD80, the majority of murine splenic B-1 cells were found to activated prior to any LPS stimulation in vitro. In contrast, the B-2 subset showed significant increase in CD80 expression only at high (≥10μg/mL) LPS concentrations. Studies of the division index of B-1 and B-2 cells showed a significant response in both subsets following stimulation with 1μg/mL and 10μg/mL LPS. However, overall, the results are inconsistent with LPS driving the preferential accumulation of B-1 cells in disease states. These experiments provided useful evidence that supported the idea that B-1 and B-2 cells respond differently to LPS. However, these studies were unable to directly address the role of P. gingivalis LPS in periodontitis. It may be that P. gingivalis LPS could have different effects to S. enteritidis LPS on primary B cells. It is still possible that B-1 cells may be more sensitive to P. gingivalis, as opposed to S. enteritidis LPS. Studies by other groups have suggested that the TH1/TH2 profile is skewed towards TH2 in chronic periodontitis and that P. gingivalis may drive this shift via its ability to signal through TLR2 (and modulate TLR4 signalling). Further, recent studies in our laboratories have found that P. gingivalis gingipains are able to polyclonally activate B cells and to break down both IFNγ and IL-12. Future studies should further examine the effects of B-1 and B-2 interactions in the mixed lymphocyte system together with subsequent studies utilising human periodontitis biopsies. The results presented in this thesis, together with work undertaken by other investigators, suggests that LPS could perturb the normal homeostatic mechanisms of the B-1 B cell-subset and increase polyclonal activation therefore contributing to the genesis of pathologies such as chronic periodontitis.
APA, Harvard, Vancouver, ISO, and other styles
3

Philips, Julia Rachel. "B-1 and B-2 B cell responses to lipopolysaccharide putative roles in the pathogenesis of periodontitis /." University of Sydney, 2006. http://hdl.handle.net/2123/1852.

Full text
Abstract:
Master of Science
Periodontal disease is one of the most widespread diseases in humans and is characterised by chronic gingival inflammation and B cell accumulation and resorption of the crest of alveolar bone with subsequent loss of teeth. Porphyromonas gingivalis has been identified as a putative aetiological agent for periodontitis. The aim of the research presented in this thesis was to investigate, using in vitro systems, the responses of autoreactive B-1 and B-2 cells to enterobacterial and nonenterobacterial lipopolysaccharide (LPS) to shed light on the pathogenesis of chronic periodontitis and other diseases involving B cell accumulation and autoantibody production. The hypotheses tested were: (1) B cells respond differently to enterobacterial and non-enterobacterial LPS. (2) B-1 cells are activated by a lower concentration of LPS than B-2 cells. (3) LPS stimulation results in preferential accumulation of B-1 cells. Findings consistent with these hypotheses would provide new evidence for different roles for B-1 and B-2 cells in immune responses and that LPS stimulation could lead to B-1 cell accumulation in diseases thus characterised. Initial experiments investigated the responses of representative B-1 (CH12) and B-2 (WEHI-279) cell lines to preparations of P. gingivalis and Salmonella enteritidis LPS utilising flow cytometric and quantitative molecular methods. The cell lines responded differently to the two LPS preparations. There were significant but limited effects on viability and proliferation in the WEHI-279 cell line, but no significant changes in mRNA expression levels for genes including Toll-like receptors (TLR2, TLR4, RP105), immunoglobulin (IgM), cytokines (IL-6, IL-10), co-stimulatory molecules (CD80, CD86), and regulators of apoptosis (Bcl-2, Bax). In the CH12 cell line however, LPS stimulation had greater effect. Addition of S. enteritidis LPS from a threshold level of 100ng/mL was found to rescue the cells from death, reflected by the percentage viability and proliferation. Stimulation of CH12 cells with S. enteritidis LPS also led to a decrease in expression of RP105 mRNA, which may be part of a negative feedback loop. Interestingly, stimulation with low concentrations P. gingivalis LPS appeared to inhibit proliferation but high LPS concentrations stimulated proliferation of CH12 cells, although no further significant effects were noted in other analyses. Evidence was found that CH12 cells have a high basal level of activation. This suggests that this line is constitutively activated. Stimulation with P. gingivalis or S. enteritidis LPS did not affect the level of CD80 mRNA expression. It is possible that the CH12 line constitutively expresses a maximal level of CD80 (and possibly CD86) and further stimulation will not cause any increase. Since S. enteritidis LPS appeared to have more pronounced effects on both B cell populations, this LPS was used to further investigate B cell subset responses in a mixed splenocyte culture system. Experiments examining percentage viability and number of viable cells indicated that B-1 and B-2 B cells responded differently to LPS stimulation. A threshold level for B-2 cell response (significant increase in cell number) was found to be 100ng/mL LPS, in contrast to the B-1 B cell subset which were only significantly different to the unstimulated cells when stimulated with 50μg/mL LPS. By examining the expression of CD80, the majority of murine splenic B-1 cells were found to activated prior to any LPS stimulation in vitro. In contrast, the B-2 subset showed significant increase in CD80 expression only at high (≥10μg/mL) LPS concentrations. Studies of the division index of B-1 and B-2 cells showed a significant response in both subsets following stimulation with 1μg/mL and 10μg/mL LPS. However, overall, the results are inconsistent with LPS driving the preferential accumulation of B-1 cells in disease states. These experiments provided useful evidence that supported the idea that B-1 and B-2 cells respond differently to LPS. However, these studies were unable to directly address the role of P. gingivalis LPS in periodontitis. It may be that P. gingivalis LPS could have different effects to S. enteritidis LPS on primary B cells. It is still possible that B-1 cells may be more sensitive to P. gingivalis, as opposed to S. enteritidis LPS. Studies by other groups have suggested that the TH1/TH2 profile is skewed towards TH2 in chronic periodontitis and that P. gingivalis may drive this shift via its ability to signal through TLR2 (and modulate TLR4 signalling). Further, recent studies in our laboratories have found that P. gingivalis gingipains are able to polyclonally activate B cells and to break down both IFNγ and IL-12. Future studies should further examine the effects of B-1 and B-2 interactions in the mixed lymphocyte system together with subsequent studies utilising human periodontitis biopsies. The results presented in this thesis, together with work undertaken by other investigators, suggests that LPS could perturb the normal homeostatic mechanisms of the B-1 B cell-subset and increase polyclonal activation therefore contributing to the genesis of pathologies such as chronic periodontitis.
APA, Harvard, Vancouver, ISO, and other styles
4

Hastings, William David. "Peritoneal B-2 cells comprise a distinct population that differentiates to a B-1b phenotype /." Citation, abstract and full text online, 2005. http://proquest.umi.com.ezproxy.bu.edu/pqdweb?did=913526461&sid=2&Fmt=2&clientId=374&RQT=309&VName=PQD.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Sherwood, Tracy. "Characterization of Cannabinoid Receptor 2 Transcript Expression in B Cells." Scholar Commons, 2010. https://scholarcommons.usf.edu/etd/1767.

Full text
Abstract:
Cannabinoids and cannabinoid receptors have been shown to play important roles in immune regulation particularly as modulators of anti-inflammatory cytokines and antibody production. The predominant cannabinoid receptor involved in this immune regulation is cannabinoid receptor 2 (CB2), which is robustly expressed in B cells. Utilizing a combination of bioinformatics, 5' RACE, real time RT-qPCR, and reporter assays, we showed that human B cells from peripheral blood mononuclear cells (PBMC) expressed one CB2 transcript while mouse B cells from spleen express three CB2 transcripts. Alignment of the sequenced B cell RACE products to either the mouse or human genome, along with the GenBank mRNA sequences, revealed that the transcripts isolated in this study contained previously unidentified transcriptional start sites (TSSs). In addition, expression construct testing of the genomic region containing the TSSs of the mouse CB2 exon 1 and 2 transcripts showed a significant increase of promoter activity. Bioinformatics analysis for cis-sequences in the promoter regions identified DNA binding sites for NF-kB, STAT6, and Elk1 transcription factors activated by LPS, IL-4 and anti-CD40. Regarding variations in CB2 transcript expression among the immune cell subtypes, RACE analysis showed that the exon 1b transcript is seen in B cells but not in T cells, dendritic cells or macrophages. Furthermore, RT-qPCR showed variations in transcript expression during B cell development as well as in resting versus LPS or IL-4/anti-CD40 stimulated B cells. The exon 1a transcript was predominant in pre-, immature and resting B cells whereas the exon 1b and 2 transcripts were enhanced in mature and activated B cells. These data showed for the first time that human B cells use one TSS for CB2 expression while mouse B cells use multiple TSSs for the expression of three CB2 transcripts, in which the expression of the individual transcript is related to immune cell type and/or cell activation state. Additionally, this is the first report in mouse B cells defining TSSs that are in genomic areas with promoter activity thus suggesting the location of two promoter regions. Defining the CB2 transcript expression during various stages of B cell activation provide clues to therapeutic methods.
APA, Harvard, Vancouver, ISO, and other styles
6

Campbell, Michelle. "The immunomodulatory role of proteinase activated receptor-2 (PAR-2) in B cells." Thesis, University of the West of Scotland, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.627909.

Full text
Abstract:
Proteinase activated receptor-2 (PAR-2) is a seven transmembrane G protein coupled receptor (GPCR) which is activated by proteolytic cleavage to reveal a cryptic tethered ligand (Macfarlane et al, 2001). Whilst PAR-2 expression has been demonstrated in a number of immune related cells (Shpacovitch et al, 2008) and has been shown on human synovial B cells (Busso et al, 2007) however a functional role for the receptor has not been proposed. Previous studies have demonstrated the benefit of PAR-2 antagonism in inflammatory models. Utilising the antagonist ENMD-1068 as a treatment in the collagen induced arthritis (CIA) model resulted in the reduction of clinical disease severity as well as reducing the proportion of splenic B cells compared with vehicle treated mice. PAR-2 was shown to be expressed on B cell progenitors, splenic, bone marrow and peritoneal B cell subsets. Following induction of CIA this expression was up-regulated in the bone marrow Hardy fraction progenitor cells, and the innate like B cell subsets found in the peritoneum, spleen and bone marrow, consistent with up-regulated PAR-2 expression found on T cells and monocytes from patients with rheumatoid arthritis (Crilly et al, 2012b).
APA, Harvard, Vancouver, ISO, and other styles
7

Gombert, Wendy Marie. "Transcriptional regulation of the bcl-2 gene in human B cells." Thesis, King's College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.312464.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Symington, Hannah Lucy. "Mechanism of IL-2 mediated BACH2 regulation in the control of Human naive B cell differentiation into plasma cells." Thesis, Rennes 1, 2016. http://www.theses.fr/2016REN1B009.

Full text
Abstract:
La différenciation terminale des lymphocytes B qui se déroule dans les centres germinatifs des organes lymphoïdes secondaires est l’étape ultime de la réponse T dépendante et aboutit à la production de plasmocytes (PC) à longue durée de vie qui sécrètent des anticorps hautement affins spécifiques de l’antigène et caractéristiques de la réponse immune adaptative. La transition d’une cellule B naïve vers un PC est gouvernée par un réseau de régulation génique bien décrit et est largement influencée par l’intégration de stimuli externes qui contrôlent le devenir des cellules B tels que l’interaction BCR-antigène et les cytokines produites par les cellules T. La stimulation précoce des lymphocytes B humains activés par IL-2, induit la différenciation en PC via une signalisation ERK prolongée entraînant la baisse d’expression de BACH2, un facteur de transcription clef des cellules B. La répression transitoire de BACH2 est suffisante pour déclencher la différenciation en plasmablastes en l’absence d’IL-2, suggérant ainsi qu’il joue un rôle de « verrou moléculaire » de la différenciation en PC. Il est à noter que cette répression forcée de BACH2 aboutit à la production de plasmablastes caractérisés par un phénotype lymphoplasmocytaire. Ce travail de recherche s’est focalisé sur la caractérisation des mécanismes moléculaires régulant l’expression de BACH2 via la voie de signalisation ERK induite par IL-2. Nous avons identifié ELK-1 comme un médiateur de la répression de BACH2 par la voie IL-2/ERK, comme l’atteste sa capacité à se lier avec un élément de régulation d’un enhancer localisé dans l’intron 1 de BACH2, induisant ainsi la répression de l’enhancer et déverrouillant la différenciation en PC. La caractérisation de cet enhancer de BACH2 a confirmé qu’il est régulé de manière dynamique au cours de la différenciation terminale B et qu’il est localisé dans une région sujette aux mutations suggérant qu’il pourrait être impliqué dans la lymphomagenèse
The terminal differentiation of B cells, which takes places within germinal centres of secondary lymphoid organs, is the ultimate step of a T cell dependent response and results in the generation of long-lived plasma cells (PCs) that secrete protective, antigen-specific, high-affinity antibodies as part of adaptive immunity. The transition of a naive B cell into a PC is governed by a well-characterised gene regulatory network and is heavily influenced by the integration of externally received signals, including BCR-antigen binding and T cell help, such as cytokines which guide B cell fate. The early IL-2 priming of human primary activated B cells triggers PC differentiation through sustained ERK signalling resulting in the down regulation of B cell transcription factor BACH2. Transient BACH2 repression is sufficient to trigger plasmablast differentiation in the absence of IL-2 suggesting that it acts as a key lock of PC differentiation. Importantly, this enforced BACH2 repression results in the generation of plasmablasts with a lymphoplasmacytic phenotype. The focus of this thesis was to characterise the molecular mechanisms regulating BACH2 expression via the IL-2 ERK transduction pathway. We identify ELK-1 as the mediator of IL-2 ERK induced BACH2 downregulation as it binds to a regulatory enhancer element located within intron 1 of BACH2 instigating its repression and unlocking the PC programme triggering differentiation. The characterisation of this BACH2 enhancer confirms that it is dynamically regulated during PC differentiation and is located within a region targeted for mutation suggesting that it may have a potential role in lymphomagenesis
APA, Harvard, Vancouver, ISO, and other styles
9

Ceizar, Maheen. "B-cell Lymphoma-2 (Bcl-2) Is an Essential Regulator of Adult Hippocampal Neurogenesis." Thèse, Université d'Ottawa / University of Ottawa, 2012. http://hdl.handle.net/10393/23287.

Full text
Abstract:
Of the thousands of dividing progenitor cells (PCs) generated daily in the adult brain only a very small proportion survive to become mature neurons through the process of neurogenesis. Identification of the mechanisms that regulate cell death associated with neurogenesis would aid in harnessing the potential therapeutic value of PCs. Apoptosis, or programmed cell death, is suggested to regulate death of PCs in the adult brain as overexpression of B-cell lymphoma 2 (Bcl-2), an anti-apoptotic protein, enhances the survival of new neurons. To directly assess if Bcl-2 is a regulator of apoptosis in PCs, this study examined the outcome of removal of Bcl-2 from the developing PCs in the adult mouse brain. Retroviral mediated gene transfer of Cre into adult floxed Bcl-2 mice eliminated Bcl-2 from developing PCs and resulted in the complete absence of new neurons at 30 days post viral injection. Similarly, Bcl-2 removal through the use of nestin-induced conditional knockout mice resulted in reduced number of mature neurons. The function of Bcl-2 in the PCs was also dependent on Bcl-2-associated X (BAX) protein, as demonstrated by an increase in new neurons formed following viral-mediated removal of Bcl-2 in BAX knockout mice. Together these findings demonstrate that Bcl-2 is an essential regulator of neurogenesis in the adult hippocampus.
APA, Harvard, Vancouver, ISO, and other styles
10

Stein, Merle [Verfasser], and Hans-Martin [Gutachter] Jäck. "A defined mitochondrial metabolic state in pre-B cells contributes to B cell homeostasis and is modulated by Swiprosin-2 / EFhd1 / Merle Stein ; Gutachter: Hans-Martin Jäck." Erlangen : Friedrich-Alexander-Universität Erlangen-Nürnberg (FAU), 2016. http://d-nb.info/1114989932/34.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "B-2 B cells"

1

Battaglini, Michelina. Determination of the transforming growth factor-B (TGF-B) receptor on the surface of interleukin-2 activated natural killer (IANK) cells. Sudbury, Ont: Laurentian University, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Lane, Peter John Lockwood. Recruitment of virgin and mature B cells into antibody responses against thymus-dependent (TD) and independent (TI-2) forms of the hapten 2,4 dinitrophenyl (DNP). Birmingham: University of Birmingham, 1986.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

Glasier, Mary-Ann M. A role for SHP-1 and Vav in the abrogation of B cell receptor signal transduction by latent membrane protein 2 (LMP2). Ottawa: National Library of Canada = Bibliothèque nationale du Canada, 1999.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
4

Regulation of the transcription factors Oct-2 and NF-[kappa]B during pre-B cell differentiation. 1993.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
5

Rosado, Maria Manuela, Marcella Visentini, Sven Geissler, Alessandro Camponeschi, and Alaitz Aranburu, eds. The B-Side of B Cells. Frontiers Media SA, 2021. http://dx.doi.org/10.3389/978-2-88971-520-6.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Chu, Yiwei, Damo Xu, and Luman Wang, eds. Insights into Regulatory B Cells. Frontiers Media SA, 2022. http://dx.doi.org/10.3389/978-2-88976-155-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Molecular Biology of B Cells. Elsevier, 2004. http://dx.doi.org/10.1016/b978-0-12-053641-2.x5000-x.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Gibbins, Jonathan M., and Martyn P. Mahaut-Smith. Platelets and Megakaryocytes : Volume 2: Perspectives and Techniques. Humana Press, 2010.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
9

Casali, Paolo, ed. Epigenetics of B Cells and Antibody Responses. Frontiers Media SA, 2016. http://dx.doi.org/10.3389/978-2-88919-790-3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Lloyd, Peter, Sarah Doaty, and Bevra H. Hahn. Aetiopathogenesis of systemic lupus erythematosus. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780198739180.003.0002.

Full text
Abstract:
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized by the presence of immune dysregulation, autoreactive B and T cells, and the production of a broad, heterogeneous group of autoantibodies (autoAb). The pathogenesis of lupus can be divided into three stages: 1) genetic predisposition and environmental exposures, 2) loss of tolerance, and 3) immune activation. In this chapter we will discuss the aetiopathogenesis of systemic lupus erythematosus with emphasis placed on key autoantibodies, cytokines, the innate and adaptive immune system, tolerance, NETosis, genetics and epigenetics, environmental triggers and the role of gender.
APA, Harvard, Vancouver, ISO, and other styles
More sources

Book chapters on the topic "B-2 B cells"

1

Phipps, R. P., S. J. Pollock, K. Kaur, J. Kaufman, M. A. Borrello, B. A. Graf, D. Nazarenko, et al. "Expression of Cyclooxygenase-2 and Prostaglandins by B-1 Cells and B-CLL Cells." In Current Topics in Microbiology and Immunology, 293–300. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_30.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Kieslinger, Matthias. "Maintenance of Hematopoiesis: Role of Early B Cell Factor 2." In Stem Cells and Cancer Stem Cells, Volume 4, 41–50. Dordrecht: Springer Netherlands, 2011. http://dx.doi.org/10.1007/978-94-007-2828-8_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Baumgarth, N., J. Chen, O. C. Herman, G. C. Jager, and L. A. Herzenberg. "The Role of B-1 and B-2 Cells in Immune Protection from Influenza Virus Infection." In Current Topics in Microbiology and Immunology, 163–69. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Nakagawa, N., T. Nakagawa, D. J. Volkman, H. Goldstein, J. L. Ambrus, and A. S. Fauci. "The Effects of Interleukin 2, Gamma Interferon, and B Cell Differentiation Factor on the Differentiation of Human B Cells." In The Molecular Basis of B-Cell Differentiation and Function, 59–62. Boston, MA: Springer US, 1986. http://dx.doi.org/10.1007/978-1-4684-7035-2_9.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Jung, Lawrence K. L., Toshiro Hara, and Shu Man Fu. "Detection and Functional Studies of IL-2 Receptors on Activated Human B Cells." In Leukocyte Typing II, 491–97. New York, NY: Springer New York, 1986. http://dx.doi.org/10.1007/978-1-4612-4848-4_42.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Volkman, David J., Thomas B. Nutman, Eric A. Ottesen, and Anthony S. Fauci. "Exogenous IL-2 Independent Antigen-Specific Human T Cells: Antigen-Specific Induction of Polyclonal B Cell Factors." In Human T Cell Clones, 125–33. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-4998-6_12.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Donius, Luke R., and John H. Weis. "Detection of Complement Receptors 1 and 2 on Mouse Splenic B Cells Using Flow Cytometry." In The Complement System, 305–10. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-724-2_24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Cancro, M. P., A. P. Sah, S. L. Levy, D. M. Allman, D. Constantinescu, M. R. Schmidt, and R. T. Woodland. "B cell production and turnover in CBA/Na, CBA/N and CBA/N-bcl-2 transgenic mice: xid-mediated failure among pre b cells is unaltered by bcl-2 overexpression." In Current Topics in Microbiology and Immunology, 31–38. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_4.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Koutsakos, Marios, Katherine Kedzierska, and Thi H. O. Nguyen. "Evaluation of Human Circulating T Follicular Helper Cells in Influenza- and SARS-CoV-2-Specific B Cell Immunity." In Methods in Molecular Biology, 201–9. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1736-6_17.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Gottardi, D., A. Alfarano, A. M. De Leo, A. Stacchini, L. Bergui, and F. Caligaris-Cappio. "Defective Apoptosis due to Bcl-2 Overexpression May Explain Why B-CLL Cells Accumulate in G0." In Current Topics in Microbiology and Immunology, 307–12. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_35.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "B-2 B cells"

1

Guttentag, S., Z. Zhang, P. Zhang, L. Suaud, R. Rubenstein, and M. Hubbard. "ERp29 Interactions with ProSP-B Facilitate Production of SP-B in Alveolar Type 2 Cells." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a6261.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Talbot, H., A. Abbaci, S. Saada, N. Gachard, J. Abraham, A. Jaccard, D. Bordessoule, AL Fauchais, T. Naves, and MO Jauberteau. "SPOT-008 Neurotensin receptor type 2 protects B-cell chronic lymphocytic leukaemia cells from apoptosis." In Abstracts of the 25th Biennial Congress of the European Association for Cancer Research, Amsterdam, The Netherlands, 30 June – 3 July 2018. BMJ Publishing Group Ltd, 2018. http://dx.doi.org/10.1136/esmoopen-2018-eacr25.41.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Kuttikrishnan, Shilpa, Kirti S. Prabhu, Tamam Elimat, Ashraf Khalil, Nicholas H. Oberlies, Feras Q. Alali, and Shahab Uddin. "Anticancer Activity of Neosetophomone B, An Aquatic Fungal Secondary Metabolite, Against Hematological Malignancie S." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0106.

Full text
Abstract:
Cancer is one of the most life threatening diseases, causing nearly 13% death in the worldwide. Leukemia, cancer of the hematopoetic cells is the main cause of cancer death in adults and children. Therapeutic agents used in treatment of cancer are known to have narrow therapeutic window and tendency to develop resistance against some cancer cell lines thus, proposing a need to discover some novel agents to treat cancer. In the present study we investigated the anticancer activity of Neosetophomone B(NSP-B), an aquatic fungal metabolite isolated from Neosetophoma sp against leukemic cells (K562 and U937). MTT results demonstrated a dose dependent inhibition of cell proliferation in K562 and U937 cell lines. Annexin staining using flow cytometry indicated that NSP-B treatment cause a dose dependent apoptosis in leukemic cells.Western blot analysis showed that NSP-B mediated apoptosis involves sequential activation of caspase 9, 3 and poly (ADP-ribose) polymerase (PARP) cleavage. Furthermore NSP-B treatment of leukemic cells resulted in upregulation of pro-apoptotic proteins (Bax) with downregulation of anti-apoptotic proteins ( Bcl-2 ).Thus, present study focuses on exploring the mechanism of anticancer activity of NSP-B on leukemic cells, raising the possibility of its use as a novel therapeutic agent for hematological malignancies. Results: We sought to determine whether NSP-B suppresses the growth of leukemic cell lines. We tested a panel of leukemic cell lines with different doses of NSP-B. Cell viability decreased in a concentration-dependent manner in K562 and U937 cell lines. NSP-B induced apoptosis in K562 and U937 cell lines via downregulation of anti-apoptotic proteins and enhancement of pro-apoptotic proteins. NSP-B induced the activation of caspase cascade signaling pathway. Altogether our results suggest that the NSP-B plays an important role in apoptosis in leukemic cell lines .Conclusions: Our data provides insight on anticancer activities of NSP-B in leukemic cell lines (K562 and U937). NSP-B inhibit cell viability via inducing apoptosis. The NSP-B mediated apoptosis occurs via downregulation of anti-apoptotic proteins and enhancement of pro-apototic proteins, thereby activating the caspase-cascade signaling. Further studies are required to elicit role of NSP-B in regulating molecular pathway involved in the progression of cancer. Taken together, above results suggest that NSP-B may have a future therapeutic role in leukemia and possibly other hematological malignancies.
APA, Harvard, Vancouver, ISO, and other styles
4

Lindeman, G. "Abstract TS3-1: Beyond B cells: Targeting BCL-2 pro-survival proteins in breast cancer." In Abstracts: 2018 San Antonio Breast Cancer Symposium; December 4-8, 2018; San Antonio, Texas. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-ts3-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Scharf, Stefanie, Janine Zahlten, Stefan Hippenstiel, Norbert Suttorp, and DJE PHILIPPE NGUESSAN. "Induction Of Human B-Defensins 2 And -3 In Pulmonary Epithelial Cells By Streptococcus Pneumoniae." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a3803.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Sato, S., T. Tanigami, K. Hakozaki, N. Shinmura, K. Iguchi, and K. Sakiyama. "A Flash Memory Technology for Operating Voltage Reduction and Self-Convergence of the Over Erased Cells." In 1995 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 1995. http://dx.doi.org/10.7567/ssdm.1995.b-2-2.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Huang, Jen Wei, Ming Seng Hsu, and Tzu-Chin Lin. "Organic photovoltaic cells of fully conjugated poly[2,6- (4,4-bis(2-ethylhexyl)-4H-cyclopenta[2,1-b;3,4-b';]dithiophene)-alt-4,7-(2,1,3-benzothiadiazole)] doped with fullerene." In SPIE Optical Engineering + Applications, edited by Shizhuo Yin and Ruyan Guo. SPIE, 2014. http://dx.doi.org/10.1117/12.2060787.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Kaewpaiboon, Sunisa, Titpawan Nakpheng, and Teerapol Srichana. "Biocompatibility of Polymyxin B Sulfate Based on Sodium Deoxycholate Sulfate Formulations with Kidney Cell Lines, Macrophage Cells, and Red Blood Cells." In 5th International Conference and Exhibition on Pharmaceutical Sciences and Technology 2022. Switzerland: Trans Tech Publications Ltd, 2022. http://dx.doi.org/10.4028/p-7490x3.

Full text
Abstract:
Antibiotic-resistant has emerged without new drug challenges. Polymyxin B (PMB) was the last resort therapy for multiple-drug resistant Gram-negative bacteria. However, the toxicity of PMB including nephrotoxicity (61%) and neurotoxicity (7%) was dose-limitation. PMB-based sodium deoxycholate sulfate (SDCS) formulations were prepared in the 2-different mole ratios of SDCS to PMB (5:1 and 10:1). Particle size, zeta-potential, and drug content were evaluated. The biocompatibility of PMB formulations was investigated with normal human primary renal proximal tubule epithelial cells (PCS-400-010), human kidney epithelial cell lines (HEK 293T/17), human kidney cell lines (WT 9-12), macrophage-like cells (RAW 264.7) and red blood cells (RBC). PMB formulations had smaller particle sizes and lower zeta-potential when compared to PMB. PMB content presented from 97-100% after lyophilization. PMB-SDCS formulations revealed lower toxicity to cell lines than PMB, especially SDCS: PMB (5:1) and low lysis of RBC. PMB-SDCS mixture had better biocompatibility than those PMB and SDCS alone.
APA, Harvard, Vancouver, ISO, and other styles
9

Fernandez, Isis E., Yuanyuan Shi, Avignat Patel, Andrew Goodwin, Ying Shi, Manuela Cernadas, Danielle Morse, and Ivan O. Rosas. "Syndecan-2 Ectopic Expression Promotes Resistance To TGF-B Induced Apoptosis And Enhances Malignant Features In A549 Cells." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5123.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Takebuchi, Masataka, Jun-ichiro Noda, Daisuke Tohyama, Shu Ueno, Kanji Osari, and Kuniyoshi Yoshikawa. "A Novel High Density EEPROM Cells Using Poly-Gate Hole (POLE) Structure Suitable for Low Power Applications." In 1995 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 1995. http://dx.doi.org/10.7567/ssdm.1995.b-2-1.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Reports on the topic "B-2 B cells"

1

Ficht, Thomas, Gary Splitter, Menachem Banai, and Menachem Davidson. Characterization of B. Melinensis REV 1 Attenuated Mutants. United States Department of Agriculture, December 2000. http://dx.doi.org/10.32747/2000.7580667.bard.

Full text
Abstract:
Brucella Mutagenesis (TAMU) The working hypothesis for this study was that survival of Brucella vaccines was directly related to their persistence in the host. This premise is based on previously published work detailing the survival of the currently employed vaccine strains S19 and Rev 1. The approach employed signature-tagged mutagenesis to construct mutants interrupted in individual genes, and the mouse model to identify mutants with attenuated virulence/survival. Intracellular survival in macrophages is the key to both reproductive disease in ruminants and reticuloendothelial disease observed in most other species. Therefore, the mouse model permitted selection of mutants of reduced intracellular survival that would limit their ability to cause reproductive disease in ruminants. Several classes of mutants were expected. Colonization/invasion requires gene products that enhance host-agent interaction or increase resistance to antibacterial activity in macrophages. The establishment of chronic infection requires gene products necessary for intracellular bacterial growth. Maintenance of chronic infection requires gene products that sustain a low-level metabolism during periods characterized little or no growth (1, 2). Of these mutants, the latter group was of greatest interest with regard to our originally stated premise. However, the results obtained do not necessarily support a simplistic model of vaccine efficacy, i.e., long-survival of vaccine strains provides better immunity. Our conclusion can only be that optimal vaccines will only be developed with a thorough understanding of host agent interaction, and will be preferable to the use of fortuitous isolates of unknown genetic background. Each mutant could be distinguished from among a group of mutants by PCR amplification of the signature tag (5). This approach permitted infection of mice with pools of different mutants (including the parental wild-type as a control) and identified 40 mutants with apparently defective survival characteristics that were tentatively assigned to three distinct classes or groups. Group I (n=13) contained organisms that exhibited reduced survival at two weeks post-infection. Organisms in this group were recovered at normal levels by eight weeks and were not studied further, since they may persist in the host. Group II (n=11) contained organisms that were reduced by 2 weeks post infection and remained at reduced levels at eight weeks post-infection. Group III (n=16) contained mutants that were normal at two weeks, but recovered at reduced levels at eight weeks. A subset of these mutants (n= 15) was confirmed to be attenuated in mixed infections (1:1) with the parental wild-type. One of these mutants was eliminated from consideration due to a reduced growth rate in vitro that may account for its apparent growth defect in the mouse model. Although the original plan involved construction of the mutant bank in B. melitensis Rev 1 the low transformability of this strain, prevented accumulation of the necessary number of mutants. In addition, the probability that Rev 1 already carries one genetic defect increases the likelihood that a second defect will severely compromise the survival of this organism. Once key genes have been identified, it is relatively easy to prepare the appropriate genetic constructs (knockouts) lacking these genes in B. melitensis Rev 1 or any other genetic background. The construction of "designer" vaccines is expected to improve immune protection resulting from minor sequence variation corresponding to geographically distinct isolates or to design vaccines for use in specific hosts. A.2 Mouse Model of Brucella Infection (UWISC) Interferon regulatory factor-1-deficient (IRF-1-/- mice have diverse immunodeficient phenotypes that are necessary for conferring proper immune protection to intracellular bacterial infection, such as a 90% reduction of CD8+ T cells, functionally impaired NK cells, as well as a deficiency in iNOS and IL-12p40 induction. Interestingly, IRF-1-/- mice infected with diverse Brucella abortus strains reacted differently in a death and survival manner depending on the dose of injection and the level of virulence. Notably, 50% of IRF-1-/- mice intraperitoneally infected with a sublethal dose in C57BL/6 mice, i.e., 5 x 105 CFU of virulent S2308 or the attenuated vaccine S19, died at 10 and 20 days post-infection, respectively. Interestingly, the same dose of RB51, an attenuated new vaccine strain, did not induce the death of IRF-1-/- mice for the 4 weeks of infection. IRF-1-/- mice infected with four more other genetically manipulated S2308 mutants at 5 x 105 CFU also reacted in a death or survival manner depending on the level of virulence. Splenic CFU from C57BL/6 mice infected with 5 x 105 CFU of S2308, S19, or RB51, as well as four different S2308 mutants supports the finding that reduced virulence correlates with survival Of IRF-1-/- mice. Therefore, these results suggest that IRF-1 regulation of multi-gene transcription plays a crucial role in controlling B. abortus infection, and IRF-1 mice could be used as an animal model to determine the degree of B. abortus virulence by examining death or survival. A3 Diagnostic Tests for Detection of B. melitensis Rev 1 (Kimron) In this project we developed an effective PCR tool that can distinguish between Rev1 field isolates and B. melitensis virulent field strains. This has allowed, for the first time, to monitor epidemiological outbreaks of Rev1 infection in vaccinated flocks and to clearly demonstrate horizontal transfer of the strain from vaccinated ewes to unvaccinated ones. Moreover, two human isolates were characterized as Rev1 isolates implying the risk of use of improperly controlled lots of the vaccine in the national campaign. Since atypical B. melitensis biotype 1 strains have been characterized in Israel, the PCR technique has unequivocally demonstrated that strain Rev1 has not diverted into a virulent mutant. In addition, we could demonstrate that very likely a new prototype biotype 1 strain has evolved in the Middle East compared to the classical strain 16M. All the Israeli field strains have been shown to differ from strain 16M in the PstI digestion profile of the omp2a gene sequence suggesting that the local strains were possibly developed as a separate branch of B. melitensis. Should this be confirmed these data suggest that the Rev1 vaccine may not be an optimal vaccine strain for the Israeli flocks as it shares the same omp2 PstI digestion profile as strain 16M.
APA, Harvard, Vancouver, ISO, and other styles
2

Banai, Menachem, and Gary Splitter. Molecular Characterization and Function of Brucella Immunodominant Proteins. United States Department of Agriculture, July 1993. http://dx.doi.org/10.32747/1993.7568100.bard.

Full text
Abstract:
The BARD project was a continuation of a previous BARD funded research project. It was aimed at characterization of the 12kDa immunodominant protein and subsequently the cloning and expression of the gene in E. coli. Additional immunodominant proteins were sought among genomic B. abortus expression library clones using T-lymphocyte proliferation assay as a screening method. The 12kDa protein was identified as the L7/L12 ribosomal protein demonstrating in the first time the role a structural protein may play in the development of the host's immunity against the organism. The gene was cloned from B. abortus (USA) and B. melitensis (Israel) showing identity of the oligonucleotide sequence between the two species. Further subcloning allowed expression of the protein in E. coli. While the native protein was shown to have DTH antigenicity its recombinant analog lacked this activity. In contrast the two proteins elicited lymphocyte proliferation in experimental murine brucellosis. CD4+ cells of the Th1 subset predominantly responded to this protein demonstrating the development of protective immunity (g-IFN, and IL-2) in the host. Similar results were obtained with bovine Brucella primed lymphocytes. UvrA, GroE1 and GroEs were additional Brucella immunodominant proteins that demonstrated MHC class II antigenicity. The role cytotoxic cells are playing in the clearance of brucella cells was shown using knock out mice defective either in their CD4+ or CD8+ cells. CD4+ defective mice were able to clear brucella as fast as did normal mice. In contrast mice which were defective in their CD8+ cells could not clear the organisms effectively proving the importance of this subtype cell line in development of protective immunity. The understanding of the host's immune response and the expansion of the panel of Brucella immunodominant proteins opened new avenues in vaccine design. It is now feasible to selectively use immunodominant proteins either as subunit vaccine to fortify immunity of older animals or as diagnostic reagents for the serological survaillance.
APA, Harvard, Vancouver, ISO, and other styles
3

McElwain, Terry F., Eugene Pipano, Guy H. Palmer, Varda Shkap, Stephn A. Hines, and Wendy C. Brown. Protection of Cattle against Babesiosis: Immunization against Babesia bovis with an Optimized RAP-1/Apical Complex Construct. United States Department of Agriculture, September 1999. http://dx.doi.org/10.32747/1999.7573063.bard.

Full text
Abstract:
Previous research and current efforts at control of babesiosis fall short of meeting the needs of countries where the disease is endemic, such as Israel, as well as the needs of exporting countries and countries bordering on endemic areas, such as the U.S. Our long-term goal is to develop improved methods of immunization against bovine babesiosis based on an understanding of the molecular mechanisms of immune protection and parasite targets of a protective immune response. In our previous BARD project, we established the basis for focusing on rhoptry antigens as components of a subunit vaccine against bovine babesiosis, and for additional research to better characterize rhoptry associated protein-1 (RAP-1) as a target of protective immunity. In this continuation BARD project, our objectives were to [1] optimize the immune response against RAP-1, and [2] identify additional rhoptry candidate vaccine antigens. The entire locus encoding B. bovis RAP-1 was sequenced, and the rap-1 open reading frame compared among several strains. Unlike B. bigemina, in which multiple gene copies with variant domains encode RAP-1, the B. bovis RAP-1 locus contains only two identical genes which are conserved among strains. Through testing of multiple truncated constructs of rRAP-1, one or more immunodominant T cell epitopes were mapped to the amino terminal half of RAP-1. At least one linear and one conformational B cell epitope have been demonstrated in the same amino terminal construct, which in B. bigemina RAP-1 also contains an epitope recognized by neutralizing antibody. The amine terminal half of the molecule represents the most highly conserved part of the gene family and contains motifs conserved broadly among the apicomplexa. In contrast, the carboxy terminal half of B. bovis RAP-1 is less well conserved and contains multiple repeats encoding a linear B cell epitope potentially capable of inducing an ineffective, T cell independent, type 2 immune response. Therefore, we are testing an amino terminal fragment of RAP-1 (RAP-1N) in an immunization trial in cattle. Cattle have beer immunized with RAP-1N or control antigen, and IL-12 with Ribi adjuvant. Evaluation of the immune response is ongoing, and challenge with virulent B. bovis will occur in the near future. While no new rhoptry antigens were identified, our studies did identify and characterize a new spherical body antigen (SBP3), and several heat shock proteins (HSP's). The SBP3 and HSP21 antigens stimulate T cells from immune cattle and are considered new vaccine candidates worthy of further testing. Overall, we conclude that a single RAP-1 vaccine construct representing the conserved amino terminal region of the molecule should be sufficient for immunization against all strains of B. bovis. While results of the ongoing immunization trial will direct our next research steps, results at this time are consistent with our long term goal of designing a subunit vaccine which contains only the epitopes relevant to induction of protective immunity. Parallel studies are defining the mechanisms of protective immunity. Apicomplexan protozoa, including babesiosis and malaria, cause persistent diseases for which control is inadequate. The apical organelles are defining features of these complex protozoa, and have been conserved through the evolutionary process, Past and current BARD projects on babesiosis have established the validity and potential of exploiting these conserved organelles in developing improved control methods applicable to all apicomplexan diseases.
APA, Harvard, Vancouver, ISO, and other styles
4

Barash, Itamar, J. Mina Bissell, Alexander Faerman, and Moshe Shani. Modification of Milk Composition via Transgenesis: The Role of the Extracellular Matrix in Regulating Transgene Expression. United States Department of Agriculture, July 1995. http://dx.doi.org/10.32747/1995.7570558.bard.

Full text
Abstract:
Altering milk composition via transgenesis depends on three main factors. (1) The availability of an efficient regulatory sequences for targeting transgene(s) to the mammary gland; (2) a reliable in vitro model to test the expression of transgenes prior to their introduction to the animal genome; and (3) better understanding of the major factors which determine the rate of gene expression and protein synthesis. The current studies provide the necessary means and knowledge to alter milk protein composition via transgenesis. The following specific goals were achieved: a: Identifying regulatory regions in the b-lactoglobulin (BLG) gene and the cross-talk between elements which enabled us to construct an efficient vector for the expression of desirable cDNA's in the mammary gland. b: The establishment of a sheep mammary cell line that serves as a model for the analysis of endogenous and exogenous milk protein synthesis in the mammary gland of livestock. c: An accurate comparison of the potency of the 5' regulatory sequences from the BLG and whey acidic protein (WAP) promoters in directing the expression of human serum albumin (HSA) to the mammary gland in vitro and in vivo. In this study we have also shown that sequences within the coding region may determine a specific pattern of expression for the transgene, distinct from that of the native milk protein genes. d: Characterizing the dominant role of ECM in transgene expression in mammary epithelial cells. e: Further characterization of the BCE-1 enhancer element in the promoter of the b-casein gene as a binding site for the c/EBP-b and Stat5. Identifying its interaction with chromatin and its up regulation by inhibitors of histone deacetylation. f: Identifying a mechanism of translational control as a mediator for the synergistic effect of insulin and prolactin on protein synthesis in the mammary gland.
APA, Harvard, Vancouver, ISO, and other styles
5

Shani, Moshe, and C. P. Emerson. Genetic Manipulation of the Adipose Tissue via Transgenesis. United States Department of Agriculture, April 1995. http://dx.doi.org/10.32747/1995.7604929.bard.

Full text
Abstract:
The long term goal of this study was to reduce caloric and fat content of beef and other red meats by means of genetic modification of the animal such that fat would not be accumulated. This was attempted by introducing into the germ line myogenic regulatory genes that would convert fat tissue to skeletal muscle. We first determined the consequences of ectopic expression of the myogenic regulatory gene MyoD1. It was found that deregulation of MyoD1 did not result in ectopic skeletal muscle formation but rather led to embryonic lethalities, probably due to its role in the control of the cell cycle. This indicated that MyoD1 should be placed under stringent control to allow survival. Embryonic lethalities were also observed when the regulatory elements of the adipose-specific gene adipsin directed the expression of MyoD1 or myogenin cDNAs, suggesting that these sequences are probably not strong enough to confer tissue specificity. To determine the specificity of the control elements of another fat specific gene (adipocyte protein 2-aP2), we fused them to the bacterial b-galactosidase reporter gene and established stable transgenic strains. The expression of the reporter gene in none of the strains was adipose specific. Each strain displayed a unique pattern of expression in various cell lineages. Most exciting results were obtained in a transgenic strain in which cells migrating from the ventro-lateral edge of the dermomyotome of developing somites to populate the limb buds with myoblasts were specifically stained for lacZ. Since the control sequences of the adipsin or aP2 genes did not confer fat specificity in transgenic mice we have taken both molecular and genetic approaches as an initial effort to identify genes important in the conversion of a multipotential cell such as C3H10T1/2 cell to adipoblast. Several novel adipocyte cell lines have been established that differ in the expression of transcription factors of the C/EBP family known to be markers for adipocyte differentiation. These studies revealed that one of the genetic programming changes which occur during 10T1/2 conversion from multipotential cell to a committed adipoblast is the ability to linduce C/EBPa gene expression. It is expected that further analysis of this gene would identify elements which regulate this lineage-specific expression. Such elements might be good candidates in future attempts to convert adipoblasts to skeletal muscle cells in vivo.
APA, Harvard, Vancouver, ISO, and other styles
6

Splitter, Gary, and Menachem Banai. Microarray Analysis of Brucella melitensis Pathogenesis. United States Department of Agriculture, 2006. http://dx.doi.org/10.32747/2006.7709884.bard.

Full text
Abstract:
Original Objectives 1. To determine the Brucella genes that lead to chronic macrophage infection. 2. To identify Brucella genes that contribute to infection. 3. To confirm the importance of Brucella genes in macrophages and placental cells by mutational analysis. Background Brucella spp. is a Gram-negative facultative intracellular bacterium that infects ruminants causing abortion or birth of severely debilitated animals. Brucellosis continues in Israel, caused by B. melitensis despite an intensive eradication campaign. Problems with the Rev1 vaccine emphasize the need for a greater understanding of Brucella pathogenesis that could improve vaccine designs. Virulent Brucella has developed a successful strategy for survival in its host and transmission to other hosts. To invade the host, virulent Brucella establishes an intracellular niche within macrophages avoiding macrophage killing, ensuring its long-term survival. Then, to exit the host, Brucella uses placenta where it replicates to high numbers resulting in abortion. Also, Brucella traffics to the mammary gland where it is secreted in milk. Missing from our understanding of brucellosis is the surprisingly lillie basic information detailing the mechanisms that permit bacterial persistence in infected macrophages (chronic infection) and dissemination to other animals from infected placental cells and milk (acute infection). Microarray analysis is a powerful approach to determine global gene expression in bacteria. The close genomic similarities of Brucella species and our recent comparative genomic studies of Brucella species using our B. melitensis microarray, suqqests that the data obtained from studying B. melitensis 16M would enable understanding the pathogenicity of other Brucella organisms, particularly the diverse B. melitensis variants that confound Brucella eradication in Israel. Conclusions Results from our BARD studies have identified previously unknown mechanisms of Brucella melitensis pathogenesis- i.e., response to blue light, quorum sensing, second messenger signaling by cyclic di-GMP, the importance of genomic island 2 for lipopolysaccharide in the outer bacterial membrane, and the role of a TIR domain containing protein that mimics a host intracellular signaling molecule. Each one of these pathogenic mechanisms offers major steps in our understanding of Brucella pathogenesis. Strikingly, our molecular results have correlated well to the pathognomonic profile of the disease. We have shown that infected cattle do not elicit antibodies to the organisms at the onset of infection, in correlation to the stealth pathogenesis shown by a molecular approach. Moreover, our field studies have shown that Brucella exploit this time frame to transmit in nature by synchronizing their life cycle to the gestation cycle of their host succumbing to abortion in the last trimester of pregnancy that spreads massive numbers of organisms in the environment. Knowing the bacterial mechanisms that contribute to the virulence of Brucella in its host has initiated the agricultural opportunities for developing new vaccines and diagnostic assays as well as improving control and eradication campaigns based on herd management and linking diagnosis to the pregnancy status of the animals. Scientific and Agricultural Implications Our BARD funded studies have revealed important Brucella virulence mechanisms of pathogenesis. Our publication in Science has identified a highly novel concept where Brucella utilizes blue light to increase its virulence similar to some plant bacterial pathogens. Further, our studies have revealed bacterial second messengers that regulate virulence, quorum sensing mechanisms permitting bacteria to evaluate their environment, and a genomic island that controls synthesis of its lipopolysaccharide surface. Discussions are ongoing with a vaccine company for application of this genomic island knowledge in a Brucella vaccine by the U.S. lab. Also, our new technology of bioengineering bioluminescent Brucella has resulted in a spin-off application for diagnosis of Brucella infected animals by the Israeli lab by prioritizing bacterial diagnosis over serological diagnosis.
APA, Harvard, Vancouver, ISO, and other styles
7

Splitter, Gary A., Menachem Banai, and Jerome S. Harms. Brucella second messenger coordinates stages of infection. United States Department of Agriculture, January 2011. http://dx.doi.org/10.32747/2011.7699864.bard.

Full text
Abstract:
Aim 1: To determine levels of this second messenger in: a) B. melitensiscyclic-dimericguanosinemonophosphate-regulating mutants (BMEI1448, BMEI1453, and BMEI1520), and b) B. melitensis16M (wild type) and mutant infections of macrophages and immune competent mice. (US lab primary) Aim 2: To determine proteomic differences between Brucelladeletion mutants BMEI1453 (high cyclic-dimericguanosinemonophosphate, chronic persistent state) and BMEI1520 (low cyclicdimericguanosinemonophosphate, acute virulent state) compared to wild type B. melitensisto identify the role of this second messenger in establishing the two polar states of brucellosis. (US lab primary with synergistic assistance from the Israel lab Aim 3: Determine the level of Brucellacyclic-dimericguanosinemonophosphate and transcriptional expression from naturally infected placenta. (Israel lab primary with synergistic assistance from the US lab). B. Background Brucellaspecies are Gram-negative, facultative intracellular bacterial pathogens that cause brucellosis, the most prevalent zoonosis worldwide. Brucellosis is characterized by increased abortion, weak offspring, and decreased milk production in animals. Humans are infected with Brucellaby consuming contaminated milk products or via inhalation of aerosolized bacteria from occupational hazards. Chronic human infections can result in complications such as liver damage, orchitis, endocarditis, and arthritis. Brucellaspp. have the ability to infect both professional and non-professional phagocytes. Because of this, Brucellaencounter varied environments both throughout the body and within a cell and must adapt accordingly. To date, few virulence factors have been identified in B. melitensisand even less is known about how these virulence factors are regulated. Subsequently, little is known about how Brucellaadapt to its rapidly changing environments, and how it alternates between acute and chronic virulence. Our studies suggest that decreased concentrations of cyclic dimericguanosinemonophosphate (c-di-GMP) lead to an acute virulent state and increased concentrations of c-di-GMP lead to persistent, chronic state of B. melitensisin a mouse model of infection. We hypothesize that B. melitensisuses c-di-GMP to transition from the chronic state of an infected host to the acute, virulent stage of infection in the placenta where the bacteria prepare to infect a new host. Studies on environmental pathogens such as Vibrio choleraeand Pseudomonas aeruginosasupport a mechanism where changes in c-di-GMP levels cause the bacterium to alternate between virulent and chronic states. Little work exists on understanding the role of c-di-GMP in dangerous intracellular pathogens, like Brucellathat is a frequent pathogen in Israeli domestic animals and U.S. elk and bison. Brucellamust carefully regulate virulence factors during infection of a host to ensure proper expression at appropriate times in response to host cues. Recently, the novel secondary signaling molecule c-di-GMP has been identified as a major component of bacterial regulation and we have identified c-di-GMP as an important signaling factor in B. melitensishost adaptation. C. Major conclusions, solutions, achievements 1. The B. melitensis1453 deletion mutant has increased c-di-GMP, while the 1520 deletion mutant has decreased c-di-GMP. 2. Both mutants grow similarly in in vitro cultures; however, the 1453 mutant has a microcolony phenotype both in vitro and in vivo 3. The 1453 mutant has increased crystal violet staining suggesting biofilm formation. 4. Scanning electron microscopy revealed an abnormal coccus appearance with in increased cell area. 5. Proteomic analysis revealed the 1453 mutant possessed increased production of proteins involved in cell wall processes, cell division, and the Type IV secretion system, and a decrease in proteins involved in amino acid transport/metabolism, carbohydrate metabolism, fatty acid production, and iron acquisition suggesting less preparedness for intracellular survival. 6. RNAseq analysis of bone marrow derived macrophages infected with the mutants revealed the host immune response is greatly reduced with the 1453 mutant infection. These findings support that microlocalization of proteins involved in c-di-GMP homeostasis serve a second messenger to B. melitensisregulating functions of the bacteria during infection of the host.
APA, Harvard, Vancouver, ISO, and other styles
8

Lurie, Susan, John Labavitch, Ruth Ben-Arie, and Ken Shackel. Woolliness in Peaches and Nectarines. United States Department of Agriculture, 1995. http://dx.doi.org/10.32747/1995.7570557.bard.

Full text
Abstract:
The overall goal of the research was to understand the processes involved in the development of woolliness in peaches and nectarines. Four specific hypotheses were proposed and in the course of the research evidence was gathered t support two of them and to not support two others. The hypotheses and a summary of the evidence are outlined below. 1. That woolliness arises from an imbalance between the activities of the cell wall pectin degrading enzymes. Using 'Flavortop' nectarines and 'Hermoza' peaches as model systems, storage regimes were manipulated to induce or prevent woolliness. The expression (mRNA abundance), protein content (Western blotting), and activity of polygalacturonase (PG) and pectin esterase (PE) were followed. Expression of the enzymes was not different, but activity and the ratio between PG and PE activities were quite different in fruits developing woolliness or ripening normally. This was also examined by looking at the substrate, the pectin moiety of the cell wall, and i woolly fruit there were more high molecular weight pectins with regions of non-methylated galacturonic acid residues. Taking an in vitro approach it was found a) that PE activity was stable at 0oC while PG activity decreased; b) incubating the calcium pectate fraction of the cell wall with PE extracted from peaches caused the polymers to form a gel characteristic of the visual woolly symptoms in peaches. 2. That continued cell wall synthesis occurs during storage and contributes to structural changes i cell walls and improper dissolution and softening after storage. We tried to adapt our technique of adding 13C-glucose to fruit discs, which was used successfully to follow cell wall synthesis during tomato ripening. However, the difference in sugar content between the two fruits (4% in tomato and 12% in peach) meant that the 13C-glucose was much more diluted within the general metabolite pool. We were unable to see any cell wall synthesis which meant that either the dilution factor was too great, or that synthesis was not occurring. 3. That controlled atmosphere (CA) prevents woolliness by lowering all enzyme activities. CA was found to greatly reduce mRNA abundance of the cell wall enzymes compared to regular air storage. However, their synthesis and activity recovered during ripening after CA storage and did not after regular air storage. Therefore, CA prevented the inhibition of enzyme activation found in regular air storage. 4. That changes in cell wall turgor and membrane function are important events in the development of woolliness. Using a micro pressure probe, turgor was measured in cells of individual 'O'Henry' and 'CalRed' peaches which were woolly or healthy. The relationship between firmness and turgor was the same in both fruit conditions. These data indicate that the development and expression of woolliness are not associated with differences in membrane function, at least with regard to the factors that determine cell turgor pressure. In addition, during the period of the grant additional areas were explored. Encoglucanase, and enzyme metabolizing hemicellulose, was found to be highly expressed air stored, but not in unstored or CA stored fruit. Activity gels showed higher activity in air stored fruit as well. This is the first indication that other components of the cell wall may be involved in woolliness. The role of ethylene in woolliness development was also investigated at it was found a) that woolly fruits had decreased ability to produce ethylene, b) storing fruits in the presence of ethylene delayed the appearance of woolliness. This latter finding has implication for an inexpensive strategy for storing peaches and nectarines.
APA, Harvard, Vancouver, ISO, and other styles
9

Thomas, C. E., and B. D. James. Technology development goals for automotive fuel cell power systems. Final report, Appendix B-2. Office of Scientific and Technical Information (OSTI), July 1995. http://dx.doi.org/10.2172/155021.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Splitter, Gary, and Menachem Banai. Attenuated Brucella melitensis Rough Rev1 Vaccine. United States Department of Agriculture, January 2004. http://dx.doi.org/10.32747/2004.7585199.bard.

Full text
Abstract:
The original objectives of the proposal were: 1. Compare mutants 444 and 710 to Rev1 (parent strain), and 16M (field strain) in murine and human macrophage lines for phenotypic differences. 2. Determine in vivo virulence and survival of the mutants 444 and 710 in guinea pigs and mice. 3. Determine humoral and cell-mediated immune responses induced by mutants 444 and 710 in guinea pigs and mice. 4. Determine in vivo protection of mice and guinea pigs provided by mutants 444 and 710 compared to Rev1. Background: While human and animal brucellosis are rare in the U.S., brucellosis caused by B. melitensis remains relatively constant in Israel. Despite a national campaign to control brucellosis in Israel, the misuse of Rev1 Elberg vaccine strain among pregnant animals has produced abortion storms raising concern of human infection due to vaccine excretion in the milk. Further, some commercial Rev1 vaccine lots can: a) produce persistent infection, b) infect humans, c) be horizontally transmitted, d) cause abortion, and e) induce a persistent anti-O-polysaccharide antibody response confounding the distinction between infected and vaccinated animals. In Israel, vaccination practices have not optimally protected the milk supply from Brucella and Rev 1 vaccine can exacerbate the problem. In addition, cattle vaccinated against B. abortus are not protected against B. melitensis supporting the need for an improved vaccine. A safe vaccine used in adult animals to produce herd resistance to infection and a vaccine that can be distinguished from virulent infection is needed. A rough Rev1 vaccine would be less virulent than the parental smooth strain and permit serologic distinction between vaccinated and infected animals. Advantages of the Rev1 vaccine foundation are: 1) Rev1 vaccination of sheep and goats against B. melintensisis approved; therefore, vaccines derived from the Rev1 foundation may be readily accepted by licensing agencies as well as commercial companies, and 2) considerable data exists on Rev1vaccination and Rev1 proteins. Therefore, a post-genomic vaccine against B. melitensis based on the Rev1 foundation would provide a great advantage. Major conclusions from our work are: 1) We have determined that mutant 710 is highly attenuated in macrophages compared to virulent field strain 16M and mutant 444. 2) We have confirmed that mutant 710 is highly attenuated in guinea pigs and mice. 3) We have determined immune responses induced by mutant 710 in animals. 4) We have determined in vivo protection of mice and guinea pigs provided by mutants 444 and 710 compared to Rev1, and importantly, mutant 710 provides a high level of protection against challenge with virulent B. melitensis 16M. Thus, our data support the goals of the grant and provide the foundation for a future vaccine useful against B. melitensis in Israel. Because of patent considerations, many of our findings with 444 and 710 have not yet been published. Scientific and Agricultural Implications: Our findings support the development of a vaccine against B. melitensis based on the mutant 710. Because strain 710 is a mutant of the Elberg Rev1 vaccine, commercialization is more likely than development of an entirely new, uncharacterized Brucella mutant or strain.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'B-2 B cells' for particular source types:
Journal articles Dissertations / Theses Books
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!

To the bibliography