scholarly journals Hypothesis: Engrafted Human Bone Marrow and Blood Cells in Culture

Blood ◽  
1972 ◽  
Vol 40 (5) ◽  
pp. 754-758 ◽  
Author(s):  
Hans W. von Heyden ◽  
George E. Moore
Keyword(s):  
Bone Marrow ◽  
Epstein Barr Virus ◽  
Lymphoblastic Leukemia ◽  
Growth Potential ◽  
Barr Virus ◽  
Before And After ◽  
Immunosuppressed Patients ◽  
Epstein Barr ◽  
Lymphoid Cell Lines

Abstract Lymphoblasts appearing in immunosuppressed patients after bone marrow transfusion are compared to those that can be established in vitro as permanent lymphoid cell lines. It is suggested that Epstein-Barr virus (EBV) could be responsible for the recurrent "lymphoblastic leukemia" in these patients and that the transplanted cells may be a clone of nonmalignant cells that has become capable of growing without normal restraints. It is important that in future patients the transplanted cells be characterized as to morphology, chromosome constitution, relative clonability and transplantability, the presence of EBV, T or B cell-like traits, and their growth potential in immunosuppressed heterologous hosts. The antibody titer to EBV should be measured before and after leukocyte transfusion.

scholarly journals Epstein-Barr virus transformation of human pre-B cells.

1983 ◽  
Vol 158 (2) ◽  
pp. 616-622 ◽  
Author(s):  
M Hansson ◽  
K Falk ◽  
I Ernberg
Keyword(s):  
Bone Marrow ◽  
B Cells ◽  
B Cell ◽  
Cell Lines ◽  
Epstein Barr Virus ◽  
Bone Marrow Cells ◽  
Fetal Bone ◽  
Barr Virus ◽  
Epstein Barr

In vitro infection of human B lymphocytes with Epstein-Barr virus (EBV) results in establishment of B lymphoblastoid cell lines that reflect normal B cell phenotypes. In this study we have investigated whether immature B cells from fetal bone marrow and liver can serve as targets for EBV. The fetal bone marrow cells were readily transformed by EBV. Among the resulting cell lines, five were surface Ig (sIg)-negative. Three B cell-associated antigens defined by monoclonal antibodies were expressed to the same extent on the fetal cell lines, whether they belonged to the sIg- or sIg+ group. The various differentiation stages that these cell lines may represent are discussed.

Glucocorticoids promote the proliferation and antagonize the retinoic acid–mediated growth suppression of Epstein-Barr virus–immortalized B lymphocytes

Blood ◽  
2000 ◽  
Vol 96 (2) ◽  
pp. 711-718 ◽  
Author(s):  
Michele Quaia ◽  
Paola Zancai ◽  
Roberta Cariati ◽  
Silvana Rizzo ◽  
Mauro Boiocchi ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Growth Inhibition ◽  
Epstein Barr Virus ◽  
Therapeutic Potential ◽  
Growth Arrest ◽  
Barr Virus ◽  
Immunosuppressed Patients ◽  
Epstein Barr

Abstract Glucocorticoids are able to release Epstein-Barr virus–immortalized (EBV-immortalized) lymphoblastoid B cell lines (LCLs) from the persistent growth arrest induced in these cells by retinoic acid (RA). Moreover, physiologic concentrations of glucocorticoids efficiently antagonized LCL growth inhibition induced by 13-cis-RA; 9-cis-RA; all-trans-RA; and Ro 40-6055, an RA  receptor (RAR) selective agonist. RAR expression levels, however, were not affected by glucocorticoids. Glucocorticoids, but not other steroid hormones, directly promote LCL proliferation, a phenomenon that was mainly mediated by down-regulation of the cyclin-dependent kinase (CDK) inhibitor p27Kip-1. Moreover, glucocorticoids contrasted the up-regulation of p27Kip-1, which was underlying the RA-induced LCL growth arrest, thereby indicating that glucocorticoids and RA signalings probably converge on p27Kip-1. Both antagonism of RA-mediated growth inhibition and promotion of LCL proliferation were efficiently reversed by the glucocorticoid receptor (GR) antagonist RU486, indicating that all of these effects were mediated by GR. Of note, RU486 also proved to be effective in vivo and, in mice, was able to significantly inhibit the growth of untreated LCLs as well as LCLs growth-arrested by RA in vitro. These findings provide a rational background to further evaluate the possible role of glucocorticoids in the pathogenesis of EBV-related lymphoproliferations of immunosuppressed patients. Moreover, GR antagonists deserve further consideration for their possible efficacy in the management of these disorders, and the use of schedules, including both RA and a GR antagonist, may allow a more thorough evaluation of the therapeutic potential of RA in this setting.

Glucocorticoids promote the proliferation and antagonize the retinoic acid–mediated growth suppression of Epstein-Barr virus–immortalized B lymphocytes

Blood ◽  
2000 ◽  
Vol 96 (2) ◽  
pp. 711-718 ◽  
Author(s):  
Michele Quaia ◽  
Paola Zancai ◽  
Roberta Cariati ◽  
Silvana Rizzo ◽  
Mauro Boiocchi ◽  
...  
Keyword(s):  
Retinoic Acid ◽  
Growth Inhibition ◽  
Epstein Barr Virus ◽  
Therapeutic Potential ◽  
Growth Arrest ◽  
Barr Virus ◽  
Immunosuppressed Patients ◽  
Epstein Barr

Glucocorticoids are able to release Epstein-Barr virus–immortalized (EBV-immortalized) lymphoblastoid B cell lines (LCLs) from the persistent growth arrest induced in these cells by retinoic acid (RA). Moreover, physiologic concentrations of glucocorticoids efficiently antagonized LCL growth inhibition induced by 13-cis-RA; 9-cis-RA; all-trans-RA; and Ro 40-6055, an RA  receptor (RAR) selective agonist. RAR expression levels, however, were not affected by glucocorticoids. Glucocorticoids, but not other steroid hormones, directly promote LCL proliferation, a phenomenon that was mainly mediated by down-regulation of the cyclin-dependent kinase (CDK) inhibitor p27Kip-1. Moreover, glucocorticoids contrasted the up-regulation of p27Kip-1, which was underlying the RA-induced LCL growth arrest, thereby indicating that glucocorticoids and RA signalings probably converge on p27Kip-1. Both antagonism of RA-mediated growth inhibition and promotion of LCL proliferation were efficiently reversed by the glucocorticoid receptor (GR) antagonist RU486, indicating that all of these effects were mediated by GR. Of note, RU486 also proved to be effective in vivo and, in mice, was able to significantly inhibit the growth of untreated LCLs as well as LCLs growth-arrested by RA in vitro. These findings provide a rational background to further evaluate the possible role of glucocorticoids in the pathogenesis of EBV-related lymphoproliferations of immunosuppressed patients. Moreover, GR antagonists deserve further consideration for their possible efficacy in the management of these disorders, and the use of schedules, including both RA and a GR antagonist, may allow a more thorough evaluation of the therapeutic potential of RA in this setting.

scholarly journals Necropsy Findings in Rhesus Monkeys Experimentally Infected with Cultured Simian Immunodeficiency Virus (SIV)/Delta

1988 ◽  
Vol 25 (6) ◽  
pp. 456-467 ◽  
Author(s):  
G. B. Baskin ◽  
M. Murphey-Corb ◽  
E. A. Watson ◽  
L. N. Martin
Keyword(s):  
Bone Marrow ◽  
Simian Immunodeficiency Virus ◽  
Rhesus Monkeys ◽  
Epstein Barr Virus ◽  
Enteric Disease ◽  
Barr Virus ◽  
Immunodeficiency Virus ◽  
Single Animal ◽  
Epstein Barr

Lesions induced in rhesus monkeys by different isolates of simian immunodeficiency virus (SIV)/Delta were studied at necropsy. Four groups of monkeys were inoculated with SIV/Delta isolated from other experimentally infected rhesus monkeys, while one group was inoculated with SIV/Delta from an asymptomatic mangabey monkey. Three rhesus isolates and the mangabey isolate were virulent, killing 75–100% of infected monkeys. One rhesus isolate, which had been extensively passaged in vitro, was attenuated but was restored to virulence by single animal passage. Clinically, infected monkeys had lymphadenopathy, splenomegaly, diarrhea, and a rash. Most monkeys died of enteric disease. The following lesions were seen: weight loss, thymic atrophy, lymphoid atrophy, bone marrow hyperplasia, encephalitis, colitis, amyloidosis, hepatitis, glomerulosclerosis, and the presence of syncytial cells. One Rh Epstein-Barr virus (EBV)-related lymphoma occurred. Opportunistic agents were identified: cytomegalovirus, adenovirus, Cryptosporidia, and Pneumocystis. Shigella and Campylobacter often caused colitis.

scholarly journals Noncytotoxic and Antitumour-Promoting Activities of Garcinia Acid Esters fromGarcinia atroviridisGriff. ex T. Anders (Guttiferae)

2012 ◽  
Vol 2012 ◽  
pp. 1-5 ◽  
Author(s):  
Mukram M. Mackeen ◽  
Lim Y. Mooi ◽  
Mohidin Amran ◽  
Nashriyah Mat ◽  
Nordin H. Lajis ◽  
...  
Keyword(s):  
Epstein Barr Virus ◽  
Antioxidant Activities ◽  
Lymphoblastic Leukemia ◽  
Early Antigen ◽  
Chemopreventive Agents ◽  
Barr Virus ◽  
Epstein Barr ◽  
Derivatives Of ◽  
Acid Esters

Thein vitroantitumour-promoting, cytotoxic, and antioxidant activities of two ester derivatives of garcinia acid, that is, 2-(butoxycarbonylmethyl)-3-butoxycarbonyl-2-hydroxy-3-propanolide (1) and 1′,1′′-dibutyl methyl hydroxycitrate (2), that had been previously isolated from the fruits ofGarcinia atroviridisGriff. ex T. Anders (Guttiferae), were examined. Based on the inhibition of Epstein-Barr virus early antigen (EBV-EA) activation, compound1(IC50: 70 μM) showed much higher (8-fold) antitumour-promoting activity than compound2(IC50: 560 μM). In addition, both compounds were nontoxic towards CEM-SS (human T-lymphoblastic leukemia) cells (CD50: >100 μM), Raji (human B-lymphoblastoid) cells (CD50: >600 μM), and brine shrimp (LD50: >300 μM). Although the antitumour-promoting activity of compound1is moderate compared with the known antitumour promoter genistein, its non-toxicity suggests the potential of compound1and related structures as chemopreventive agents. The weak antioxidant activity displayed by both compounds also suggested that the primary antitumour-promoting mechanism of compound1did not involve oxidative-stress quenching.

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