Academic literature on the topic 'B-1 B cells'
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Journal articles on the topic "B-1 B cells"
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Yeo, Seung Geun, Joong Saeng Cho, Dong Choon Park, and Thomas L. Rothstein. "B-1 Cells Differ from Conventional B (B-2) Cells: Difference in Proliferation." Immune Network 4, no. 3 (2004): 155. http://dx.doi.org/10.4110/in.2004.4.3.155.
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Montecino-Rodriguez, Encarnacion, and Kenneth Dorshkind. "Formation of B-1 B Cells from Neonatal B-1 Transitional Cells Exhibits NF-κB Redundancy." Journal of Immunology 187, no. 11 (October 26, 2011): 5712–19. http://dx.doi.org/10.4049/jimmunol.1102416.
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Popi, Ana Flavia. "B-1 phagocytes: the myeloid face of B-1 cells." Annals of the New York Academy of Sciences 1362, no. 1 (July 6, 2015): 86–97. http://dx.doi.org/10.1111/nyas.12814.
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Savitsky, David, and Kathryn Calame. "B-1 B lymphocytes require Blimp-1 for immunoglobulin secretion." Journal of Experimental Medicine 203, no. 10 (September 5, 2006): 2305–14. http://dx.doi.org/10.1084/jem.20060411.
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B-1 B cells produce circulating natural antibodies that provide “innate-like” protection against bacterial and viral pathogens. They also provide adaptive responses to blood and air-borne pathogens. B lymphocyte–induced maturation protein 1 (Blimp-1) is a transcriptional repressor that is required for the formation of B-2–derived antibody-secreting plasma cells. In this study, we used mice lacking Blimp-1 in the B cell lineage to show that Blimp-1 is not necessary for the formation or self-renewal of B-1 B cells but that Blimp-1 is required for normal immunoglobulin (Ig) secretion by B-1 cells. B-1 cells lacking Blimp-1 do not repress Pax5 mRNA and do not induce X-box binding protein 1, and μ secreted mRNA normally, showing that B-1 and B-2 cells both use a common pathway for Ig secretion. Blimp-1–deficient B-1 B cells are also defective in providing early protection against influenza infection.
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Quách, Tâm D., Thomas J. Hopkins, Nichol E. Holodick, Raja Vuyyuru, Tim Manser, Ruthee-Lu Bayer, and Thomas L. Rothstein. "Human B-1 and B-2 B Cells Develop from Lin−CD34+CD38loStem Cells." Journal of Immunology 197, no. 10 (October 7, 2016): 3950–58. http://dx.doi.org/10.4049/jimmunol.1600630.
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Kantor, Aaron B. "The development and repertoire of B-1 cells (CD5 B cells)." Immunology Today 12, no. 11 (November 1991): 389–91. http://dx.doi.org/10.1016/0167-5699(91)90136-h.
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HASTINGS, W., S. GURDAK, J. TUMANG, and T. ROTHSTEIN. "CD5+/Mac-1− peritoneal B cells: A novel B cell subset that exhibits characteristics of B-1 cells." Immunology Letters 105, no. 1 (May 15, 2006): 90–96. http://dx.doi.org/10.1016/j.imlet.2006.01.002.
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Rabin, E. M., J. Ohara, and W. E. Paul. "B-cell stimulatory factor 1 activates resting B cells." Proceedings of the National Academy of Sciences 82, no. 9 (May 1, 1985): 2935–39. http://dx.doi.org/10.1073/pnas.82.9.2935.
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MURAKAMI, MASAO, and TASUKU HONJO. "B-1 Cells and Autoimmunitya." Annals of the New York Academy of Sciences 764, no. 1 (June 28, 2008): 402–9. http://dx.doi.org/10.1111/j.1749-6632.1995.tb55855.x.
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Sindhava, Vishal J., and Subbarao Bondada. "Autoregulatory B-1 cells (34.13)." Journal of Immunology 182, no. 1_Supplement (April 1, 2009): 34.13. http://dx.doi.org/10.4049/jimmunol.182.supp.34.13.
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Abstract Immunological tolerance in the periphery is mediated by clonal inactivation mechanisms as well as by regulatory cells. Recent studies showed that high IL-10 producing B-cell subsets with varying phenotype can regulate different immune responses in numerous mouse models. We found that, in comparison to B-2 cells, peritoneal B-1a cells are hyporesponsive to TLR stimulation in proliferation and antibody secretion, but produce very high amounts of IL-10. We hypothesized that the high IL-10 levels work in an autocrine manner and autoregulate B-1 cells that are prone to produce autoantibodies. Accordingly, neutralization of IL-10 enhanced peritoneal B-1, but not splenic B-2 cell proliferation and differentiation to all TLRs tested. Moreover, IL-10-/- peritoneal B-1 B-cells responded better than wild type B-1 cells to TLR stimulation. Co-stimulation with CD40 and BAFF, but not IL-5, overcame the inhibitory effect of IL-10. The increased IL-10 production was unique to peritoneal B-1 B-cells, since splenic B-1 B cells behaved like splenic B-2 cells, in terms of IL-10 production and proliferation. This autoregulation appears to have physiological significance since IL-10 knock out peritoneal B-1 cells controlled Borrelia hermsii infection better than wild type B-1 cells. Thus the IL-10 mediated autoregulation of B-1 cells may have a role in the control of autoimmunity and infection. (Supported by NIH grants to SB).
Dissertations / Theses on the topic "B-1 B cells"
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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.
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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.
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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 textAbstract:
Master of SciencePeriodontal 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.
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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 textAbstract:
Master of SciencePeriodontal 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.
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Chen, Hui-Chen. "Role for cyclic adenosine monophosphate (cAMP) response element binding proteins in B lymphocyte development and functional maturation." Connect to this title online, 2003. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1061213266.
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Thesis (Ph. D.)--Ohio State University, 2003.Document formatted into pages. Includes bibliographical references. Abstract available online via OhioLINK's ETD Center; full text release delayed at author's request until 2005 Aug. 19.
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Kazbay, Kasim. "Leu 1+B cells in autoimmune human diseases." Thesis, McGill University, 1989. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55681.
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Le, Thuc-vy L. "B cell clonal abundance and madcam-1 mediate affinity maturation and fate of germinal center B cells." Thesis, Birmingham, Ala. : University of Alabama at Birmingham, 2007. https://www.mhsl.uab.edu/dt/2009r/le.pdf.
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Zao, Chih-Ling. "B Virus Circumvents Innate Responses in Human Cells." Digital Archive @ GSU, 2008. http://digitalarchive.gsu.edu/biology_diss/41.
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B virus (Cercopithecine herpesvirus 1) is an alphaherpesvirus indigenous to macaque monkeys and is closely related to herpes simplex virus type 1 (HSV-1). Disease caused by B virus, which is often mild or asymptomatic in its natural host, the macaque monkey, is similar in infected macaques to HSV-1 infection in humans. When B virus zoonotically infects foreign hosts, e.g., humans, high morbidity and mortality are evidenced in > 80% of untreated cases. To explore the underlying reasons for differences in pathogenesis between B virus and HSV-1 infection in humans, human microarrays were used to comparatively examine global cellular gene expression patterns engaged as a result of infection of human foreskin fibroblasts (HFFs). Our results demonstrate that these closely related simplexvirus family members have divergent strategies to thwart host cell pathways related to innate defenses. In these studies, B virus did not induce detectable interferon, cytokine or chemokine genes, in sharp contrast to HSV-1, which induced innate immune responsive genes in infected cells. Although no innate immune response genes were found to be up-regulated by B virus infection, B virus induced I£eB£a, which was the only gene found to be involved in the NF-£eB signaling pathway within the innate immunity biological network. Quantification of NF-£eB p50 DNA binding activity in virus-infected nuclear extracts demonstrated that NF-£eB p50 DNA binding activity was lower in B virus-infected cells. Suppression of I£eB£a in B virus infected cells by siRNA restored NF-£eB-induced cytokine and chemokine expressions. Data presented here support the model that I£eB£a inhibits NF-£eB regulated immune responsive genes in B virus-infected HFF cells, and this response differs from that observed in HFF cells infected with HSV-1. The result is that B virus alters the NF-£eB regulated expression of cytokine and chemokine genes of HFF cells differently from HSV-1 early after infection. These differences in cytokine and chemokine expression may be associated with the delayed or reduced host responses observed in B virus infected humans and underlie the failure of adaptive responses in zoonotically infected humans.
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Cox, Selwyn Lewis Garvan Institute of Medical Research Faculty of Medicine UNSW. "The role of B cells in type 1 diabetes." Publisher:University of New South Wales. Garvan Institute of Medical Research, 2009. http://handle.unsw.edu.au/1959.4/43789.
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Type 1 Diabetes (T1D) is an autoimmune disease where the immune system destroys the insulin-producing beta cells within the pancreas. Due to the difficulty of obtaining relevant tissue samples from patients at risk of disease, many researchers have utilized the nonobese diabetic (NOD) mouse as a model of T1D due to their natural high susceptibility for this disease which shares many characteristics with human patients. This model has been critical for uncovering many mechanisms involved in the pathogenesis of T1D including the key roles played by autoreactive T cells in the destruction of beta cells. More recently, NOD mice have shown that self-reactive B cells act as important antigen presenting cells for activating and amplifying the T cell response against beta cells. In order to identify faulty self-tolerance mechanisms causing production and activation of B cells recognizing beta cell proteins, we have developed a transgenic mouse model whereby elevated numbers of B cells are made specific for a neo-self antigen whose expression is restricted to beta cells on the T1D-prone NOD genetic background and compared it to that of transgenic mice of the non-autoimmune prone C57BL/6 (B6) genetic background. These studies revealed that NOD and B6 B cells can both be effectively tolerized to the model beta cell-restricted antigen. However, provision of help from activated T cells readily overturned this tolerance on the NOD but not the B6 background. Prior evidence has associated Idd5 (chromosome 1) and Idd9/11 (chromosome 4) diabetes susceptibility loci in NOD mice with the development of self reactive B cells contributing to T1D. The gene encoding CTLA-4 has been identified as the major candidate susceptibility gene within Idd5, thus leading to our studies comparing B cell expression of this molecule in NOD and diabetes-resistant strains. Although almost always associated with down-modulating T cells responses, our studies and that of others confirm expression of CTLA-4 by activated B cells. We encountered B cell expression of CTLA-4 to vary from that of T cells, being expressed earlier and predominantly on the cell surface rather than within intracellular vesicles. Our studies also showed aberrant expression of different splice variants of CTLA-4 by NOD B cells compared to diabetes-resistant mice controlled by genes within and outside the Idd5 genetic locus. Hence, these studies raise the possibility that CTLA-4 may contribute to T1D through its actions on both T and B cells. Given the large nature of the Idd9/11 susceptibility locus in NOD mice and the absence of any strong candidate genes that may influence the diabetogenic capacity of B cells in this strain, we resorted to microarray technology to reveal putative genes within this genomic region with the potential to control the B cell phenotype. We focused our microarray studies on the first transitional (T1) B cell population in the spleen given that it is an important stage of tolerance to peripherally expressed self-antigens which have been found to possess various defects in NOD mice. Comparing gene expression profiles of NOD T1 B cells that expressed susceptibility or resistance alleles at the Idd9/11 locus identified 20 differentially expressed genes with the potential to contribute to development of diabetogenic B cells. Overall, data presented in this thesis provides a greater understanding of the molecular and cellular mechanisms underlying B cell contribution to T1D in NOD mice. These data are hoped to eventually lead to the development of selective strategies for removing or inhibiting only those B cells that contribute to development of T1D while ensuring that humoral immunity to foreign pathogens remains intact in human patients at risk of developing disease.
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Ekici, Rifat. "B cells in Type 1 diabetes : studies on cell surface antibody binding." Licentiate thesis, Umeå universitet, Immunologi/immunkemi, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-37376.
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Schneider, Dina. "The role of paired box 5, B lymphocyte-induced maturation protein-1 and activation protein-1 in the suppression of B cell differentiation by 2,3,7,8-tetrachlorodibenzo-p-dioxin." Diss., Connect to online resource - MSU authorized users, 2008.
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Thesis (Ph.D.)--Michigan State University. Dept. of Pharmacology and Toxicology, 2008.Title from PDF t.p. (viewed on Mar. 30, 2009) Includes bibliographical references (p.157-191). Also issued in print.
Books on the topic "B-1 B cells"
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Vitale, Gaetano, and Francesca Mion, eds. Regulatory B Cells. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1161-5.
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Mion, Francesca, and Silvia Tonon, eds. Regulatory B Cells. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1237-8.
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Wang, Ji-Yang, ed. B Cells in Immunity and Tolerance. Singapore: Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-3532-1.
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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.
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Houghton Mifflin Harcourt Publishing Company. Hybrid Student Resource Package Module B Grades 6-8 with 1 Year Digital 2018: Cells and Heredity. Houghton Mifflin Harcourt Publishing Company, 2018.
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HARCOURT, HOUGHTON MIFFLIN. Dimensions de LAS CIENCIAS 1 Year Digital: Student Interactive Digital Curriculum Module B Online Grades 6-8 Cells and Heredity 2018. Houghton Mifflin Harcourt Publishing Company, 2018.
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Molecular Biology of B Cells. Elsevier, 2015. http://dx.doi.org/10.1016/c2011-0-08288-1.
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Gibbins, Jonathan M., and Martyn P. Mahaut-Smith. Platelets and Megakaryocytes : Volume 1: Functional Assays. Humana Press, 2010.
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Anderson, Kenneth C., and Nikhil C. Munshi. Advances in Biology and Therapy of Multiple Myeloma : Volume 1: Basic Science. Springer London, Limited, 2012.
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Anderson, Kenneth C., and Nikhil C. Munshi. Advances in Biology and Therapy of Multiple Myeloma : Volume 1: Basic Science. Springer, 2014.
Find full textBook chapters on the topic "B-1 B cells"
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Boldison, Joanne, Larissa Camargo Da Rosa, and F. Susan Wong. "Regulatory B Cells in Type 1." In Methods in Molecular Biology, 419–35. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1237-8_22.
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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.
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Bos, N. A., J. J. Cebra, and F. G. M. Kroese. "B-1 Cells and the Intestinal Microflora." In Current Topics in Microbiology and Immunology, 211–20. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_22.
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Vidovic’, D., and Z. Dembic’. "Qa-1 Restricted γδ T Cells Can Help B Cells." In Function and Specificity of γ/δ T Cells, 239–44. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76492-9_34.
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Andrew, E., W. Annis, and R. N. Maini. "Both LY-1 B Cells And Conventional B Cells Make Autoantibodies to Bromelain-Treated Autologous Erythrocytes." In Advances in Experimental Medicine and Biology, 119–23. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5535-9_17.
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Potter, M., and F. Melchers. "Opinions on the Nature of B-1 Cells and Their Relationship to B Cell Neoplasia." In Current Topics in Microbiology and Immunology, 307–24. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_32.
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Holmes, K. L., J. S. Lee, and H. C. Morse. "Mac-1+ Bone Marrow Cells Include Precursors of B Cells and T Cells." In Current Topics in Microbiology and Immunology, 19–26. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-74006-0_4.
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MacKenzie, M. R., and T. G. Paglieroni. "B-1 (CD 5+) B-Cells as a Marker of Immune Dysregulation in Multiple Myeloma." In Current Topics in Microbiology and Immunology, 51–56. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79275-5_7.
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Berland, R., and H. H. Wortis. "Role of NFAT in the Regulation of B-1 Cells." In Current Topics in Microbiology and Immunology, 131–40. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_14.
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Bondada, S., G. Bikah, D. A. Robertson, and G. Sen. "Role of CD5 in growth regulation of B-1 cells." In Current Topics in Microbiology and Immunology, 141–49. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57284-5_15.
Full textConference papers on the topic "B-1 B cells"
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Roccaro, Aldo M., Yawara Kawano, Antonio Sacco, Jihye Park, Michele Moschetta, Yuji Mishima, Elizabeth Morgan, Ruben Carrasco, and Irene Ghobrial. "Abstract 679: Dual conditional loss of BLIMP-1 and p53 in B-cells drives B-cell lymphomagenesis." In Proceedings: AACR 107th Annual Meeting 2016; April 16-20, 2016; New Orleans, LA. American Association for Cancer Research, 2016. http://dx.doi.org/10.1158/1538-7445.am2016-679.
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Wouters, Dirk J. "Current FeRAM Technology Developments and Scaling towards 3-D Capacitor Cells." In 2003 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 2003. http://dx.doi.org/10.7567/ssdm.2003.b-1-1.
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Yamamoto, N., SM Kerfoot, T. Aoyagi, K. Inden, M. Hatta, H. Kunishima, Y. Hirakata, K. Kawakami, M. Kaku, and PW Askenase. "Transfer therapy of Immune B-1 cells triggered by activated iNKT cells for acute lung infection withS. pneumoniae." 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.a5746.
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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.
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Kao, Y., W. Hsieh, C. Chen, Y. King, and C. Lin. "Statistical Analysis of the Correlations between Cell Performance and its Initial States in CRRAM Cells." In 2016 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 2016. http://dx.doi.org/10.7567/ssdm.2016.b-1-05.
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Erlandsson, M., C. Wasen, G. Gravina, and MI Bokarewa. "P065 Insulin-like growth factor 1 receptor regulates the phenotype and function of CD21+ B cells." In 38th European Workshop for Rheumatology Research, 22–24 February 2018, Geneva, Switzerland. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-ewrr2018.84.
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Erlandsson, M., C. Wasen, G. Gravina, and M. I. Bokarewa. "THU0039 Insulin-like growth factor 1 receptor regulates the phenotype and function of cd21+ b cells." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.5300.
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Sakaruassen, K. S., J. S. Powell, E. W. Raines, and R. Ross. "SELECTIVE EXPRESSION OF PLATELET-DERIVED GROWTH FACTOR B-CHAIN mRNA BY HUMAN ENDOTHELIAL CELLS AND BY HUMAN PERIPHERAL BLOOD MONOCYTES, BUT NOT BY HUMAN SMOOTH MUSCLE CELLS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643752.
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Vascular injury may occur by a variety of mechanisms. Episodes of local hypoxia or conditions leading to local generation of thrombin may influence local cells to release growthregulatory molecules such as platelet-derivedgrowth factor (PDGF) in the surrounding connective tissue. The roles of the cells and of PDGF in these processes are not entirely understood, and this prompted us to investigate effects of hypoxia (5% O2) on cultured human saphenous vein endothelial cells andhuman thoracic aorta smooth muscle cells. Freshly isolated human peripheral blood monocytes were exposed to 3.0 U/ml a-thrombin. PDGF-A and PDGF-B mRNAs were analyzed by Northern blots, and their levels were assessed by dot blots utilizing 32P nick-translated cDNA probes. Selective expressionof PDGF-B mRNA occurred in endothelial cells during hypoxia and in monocytes exposed to thrombin. Genes coding for PDGF-A and PDGF-B are expressed cons tit utively, in endothelium, and after 48 hr of hypoxia a nine-fold increase of PDGF-B mRNA is detected (9 pg mRNA/ug total RNA). No detectable levels of mRNA encoding PDGF-A and PDGF-B were observed in freshly isolated monocytes; however, a 4-hr exposure to a-thrombin resulted in a selective and transitory increase in PDGF-B mRNA, amountingto 1 pg mRNA/ug toted RNA. No PDGF-B mRNA wasdetected after 20 hr. Hypoxic conditions did not trigger any selective expression of PDGF-B mRNA in smooth muscle, including arterialsmooth muscle derived from 1-day- and 3-month-old individuals, or from adult venous smoot muscle. However, constitutive expression of PDGF-A mRNA was observed in each of these, amounting to 0.4 pg mRNA/ug total RNA in the 1-day- and 3-month-old cells, and 0.2 pg mRNA/ugtotal RNA in the venous smooth muscle. Our datashow that endothelium and monocytes selectively express PDGF-B mRNA in vitro in response to conditions mimicking those encountered during vascular injury in some in-vivo situation.The data imply that both endothelial cells and monocyte/macrophages may be sources for mitogens that induce intimal hyperplasia and eventually plaque formation.
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Zhang, T., T. Sakanoue, and T. Takenobu. "Introducing optical resonators into polymer light-emitting electrochemical cells." In 2017 International Conference on Solid State Devices and Materials. The Japan Society of Applied Physics, 2017. http://dx.doi.org/10.7567/ssdm.2017.b-1-02.
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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.
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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.
Reports on the topic "B-1 B cells"
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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.
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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.
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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.
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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.
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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.
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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.
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Zchori-Fein, Einat, Judith K. Brown, and Nurit Katzir. Biocomplexity and Selective modulation of whitefly symbiotic composition. United States Department of Agriculture, June 2006. http://dx.doi.org/10.32747/2006.7591733.bard.
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Whiteflies are sap-sucking insects that harbor obligatory symbiotic bacteria to fulfill their dietary needs, as well as a facultative microbial community with diverse bacterial species. The sweetpotato whitefly Bemisia tabaci (Gennadius) is a severe agricultural pest in many parts of the world. This speciesconsists of several biotypes that have been distinguished largely on the basis of biochemical or molecular diagnostics, but whose biological significance is still unclear. The original objectives of the project were (i) to identify the specific complement of prokaryotic endosymbionts associated with select, well-studied, biologically and phylogeographically representative biotypes of B. tabaci, and (ii) to attempt to 'cure’ select biotypes of certain symbionts to permit assessment of the affect of curing on whitefly fitness, gene flow, host plant preference, and virus transmission competency.To identify the diversity of bacterial community associated with a suite of phylogeographically-diverseB. tabaci, a total of 107 populations were screened using general Bacteria primers for the 16S rRNA encoding gene in a PCR. Sequence comparisons with the available databases revealed the presence of bacteria classified in the: Proteobacteria (66%), Firmicutes (25.70%), Actinobacteria (3.7%), Chlamydiae (2.75%) and Bacteroidetes (<1%). Among previously identified bacteria, such as the primary symbiont Portiera aleyrodidarum, and the secondary symbionts Hamiltonella, Cardinium and Wolbachia, a Rickettsia sp. was detected for the first time in this insect family. The distribution, transmission, and localization of the Rickettsia were studied using PCR and fluorescence in situ hybridization (FISH). Rickettsia was found in all 20 Israeli B. tabaci populations screened as well as some populations screened in the Arizona laboratory, but not in all individuals within each population. FISH analysis of B. tabaci eggs, nymphs and adults, revealed a unique concentration of Rickettsia around the gut and follicle cells as well as its random distribution in the haemolymph, but absence from the primary symbiont housing cells, the bacteriocytes. Rickettsia vertical transmission on the one hand and its partial within-population infection on the other suggest a phenotype that is advantageous under certain conditions but may be deleterious enough to prevent fixation under others.To test for the possible involvement of Wolbachia and Cardiniumin the reproductive isolation of different B. tabacibiotypes, reciprocal crosses were preformed among populations of the Cardinium-infected, Wolbachia-infected and uninfected populations. The crosses results demonstrated that phylogeographically divergent B. tabaci are reproductively competent and that cytoplasmic incompatibility inducer-bacteria (Wolbachia and Cardinium) both interfered with, and/or rescued CI induced by one another, effectively facilitating bidirectional female offspring production in the latter scenario.This knowledge has implications to multitrophic interactions, gene flow, speciation, fitness, natural enemy interactions, and possibly, host preference and virus transmission. Although extensive and creative attempts undertaken in both laboratories to cure whiteflies of non-primary symbionts have failed, our finding of naturally uninfected individuals have permitted the establishment of Rickettsia-, Wolbachia- and Cardinium-freeB. tabaci lines, which are been employed to address various biological questions, including determining the role of these bacteria in whitefly host biology.
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Friedmann, Michael, Charles J. Arntzen, and Hugh S. Mason. Expression of ETEC Enterotoxin in Tomato Fruit and Development of a Prototype Transgenic Tomato for Dissemination as an Oral Vaccine in Developing Countries. United States Department of Agriculture, March 2003. http://dx.doi.org/10.32747/2003.7585203.bard.
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The broad objective of the project was to develop a feasible approach to combat diarrheal disease caused by ETEC through the development of a low-cost oral immunogen in tomato fruit, expressed in the context of a prototype tomato that would answer the shortcomings of plant oral vaccines, especially in terms of produce handling and control of gene escape. Specifically, the goals for Boyce Thompson Institute (BTI) on this project were to develop transgenic tomato lines that express the enterotoxigenic E. coli (ETEC) heat-labile enterotoxin (LT) subunits A and/or B for use in oral edible vaccines, and to optimize expression and assembly of these antigens in tomato fruits.LT-B is a useful vaccine antigen against ETEC disease, since antibodies against LT-B can prevent binding and delivery of the holotoxinLT. Mutant forms of the toxic LT-A subunit that have reduced toxicity can be co-expressed and assembled with LT-Bpentamers to form mutant LT (mLT) complexes that could be used as mucosaladjuvants for other oral vaccines. Work on the project is continuing at Arizona State University, after Dr. Mason moved there in August 2002. A number of approaches were taken to ensure the expression of both subunits and bring about their assembly inside the transgenic fruits. Initially, expression was driven by the fruit-specific E-8 promoter for LT-B and the constitutive CaMV 35S promoter for LT-A(K63). While LT-B accumulated up to 7 µg per gram ripe fruit, assembled LT-K63 was only 1 µg per gram. Since promoter activities for the two genes likely differed in cell type and developmental stage specificity, the ratios of A and B subunits was not optimal for efficient assembly in all cells. In order to maximize the chance of assembly of mLT in fruit, we focused on constructs in which both genes are driven by the same promoter. These included co-expression plasmids using the 35S promoter for both, while switching to attenuated mLTs (LT-R72 and LT-G192) that have shown greater potential for oral adjuvanticity than the initial LT-K63, and thus are better candidates for a plant-derived adjuvant. Other, more novel approaches were then attempted, including several new vectors using the tomato fruit-specific E8 promoter driving expression of both LT-B and mutant LT-A, as well as a dicistronic construct for co-expression of both LT-B and mutant LT-A genes from a single promoter, and a geminivirusreplicon construct. We describe in the Appendix the results obtained in transgenic tomato lines transformed with these constructs. Overall, each contributed to enhanced expression levels, but the assembly itself of the holotoxin to high levels was not observed in the fruit tissues. The Israeli lab’s specific objective was to develop transgenic tomato lines expressing the LTholotoxin antigen bearing attributes to prevent gene escape (male sterility and orange fruit color) and to improve the dissemination of the oral vaccine (long shelf-life tomato cherry fruit or tomato processing background). Breeding lines bearing a number of attributes to prevent gene escape were developed by combining material and backcrossing either to a tomato cherry background, or two different processing backgrounds. Concomitantly, (these lines can be utilized for the creation of any future oral vaccine or other therapeutic-expressing tomato, either by crosses or transformation), the lines were crossed to the holotoxin-expressing tomatoes received from the United States, and this transgenic material was also incorporated into the backcrossing programs. To date, we have finalized the preparation of the cherry tomato material, both non-transgenic (bearing all the desired attributes), and transgenic, expressing the holotoxin. The level of expression of LT-B in the cherry fruits was comparable to the original transgenic tomatoes. Since it was not higher, this would necessitate the consumption of more fruits to reach a desired dose. A final backcross has been made for both the non-transgenic and the transgenic material in the processing lines. Auxin sprays resulted in high percentages of fruit set, but the processing genotypes gave many puffed fruits.
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McElwain, Terry, Eugene Pipano, Guy Palmer, Varda Shkap, Stephen Hines, and Douglas Jasmer. Protection of Cattle Against Babesiosis: Immunization with Recombinant DNA Derived Apical Complex Antigens of Babesia bovis. United States Department of Agriculture, June 1995. http://dx.doi.org/10.32747/1995.7612835.bard.
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Bovine babesiosis caused by Babesia bovis continues to be a significant deterrent to global livestock production. Current control methods have both biological and technical drawbacks that have stimulated research on improved methods of vaccination. This BARD project has focused on characterization of candidate Babesia bovis vaccine antigens located in the apical complex, a unique group of subcellular organelles - including rhoptries, micronemes, and spherical bodies - involved in the invation of erythrocytes. Spherical bodies and rhoptries were partially purified and their contents characterized using monoclonal antibodies. Existing and newly developed monoclonal antibodies bound to antigens in the spherical body, rhoptry, merozoite membrane, and infected erythrocyte membrane. In an initial immunization study using biologically cloned strains, it was demonstrated that strain-common epitopes are important for inducing immune protection against heterologous challenge. Rhoptry-associated antigen 1 (RAP-1) had been demonstrated previously to induce partial immune protection, fulfilled criteria of broad interstrain B and T cell epitope conservation, and thus was further characterized. The RAP-1 gene family consists of at least two gene copies, is homologous to the RAP-1 gene family in B. bigemina, and contains significant sequence similarity to other erythroparasitic protozoan candidate vaccine antigens, including the apical membrane antigen of Plasmodium falciparum. A new RAP-1 monoclonal antibody was developed that inhibits merozoite growth in vitro, demonstrating the presence of a RAP-1 neutralization sensitive domain. Based on these observations, cattle were immunized with Mo7 (Mexico) strain recombinant RAP-1 representing one of the two gene copies. All cattle responded with variable levels of serum antibodies inhibitory to heterologous Israel strain merozoite growth in vitro, and RAP-1 specific T lymphocytes that proliferated when stimulated with either homologous or heterologous native parasite antigen. Minimal protection from clinical disease was present after virulent Israel (heterologous) strain B. bovis challenge. In total, the results support the continued development of RAP-1 as a vaccine antigen, but indicate that additional information about the native structure and function of both RAP-1 gene copies, including the relationship of conserved and polymorphic sequences to B and T cell lepitopes relevant for protection, is necessary for optimization of RAP-1 as a vaccine component.
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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.
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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.
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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 textAbstract:
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.
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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.
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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.
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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 textAbstract:
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.