51Cr Labelling of Normal Human T and B Lymphocytes for Kinetic Studies in Vivo

2009 ◽  
Vol 20 (4) ◽  
pp. 319-329 ◽  
Author(s):  
Viggo Jønsson ◽  
Bjarne Egelund Christensen
Immunobiology ◽  
1992 ◽  
Vol 185 (1) ◽  
pp. 20-27
Author(s):  
Günther Dannecker ◽  
Salaheddine Mecheri ◽  
Michael K. Hoffmann

2004 ◽  
Vol 26 (2) ◽  
pp. 83-93 ◽  
Author(s):  
Dharmendra K. V. Boppana ◽  
G. Dhinakar RAJ ◽  
Lalitha John ◽  
Stephen K. Wikel ◽  
B. R. Latha ◽  
...  

Blood ◽  
1991 ◽  
Vol 77 (1) ◽  
pp. 149-158 ◽  
Author(s):  
J Golay ◽  
A Capucci ◽  
M Arsura ◽  
M Castellano ◽  
V Rizzo ◽  
...  

Abstract The steady-state expression of three members of the myb family of genes, c-myb, B-myb, and A-myb, was studied in four purified normal human hematopoietic cell types, ie, T and B lymphocytes, monocytes, and granulocytes. The c-myb proto-oncogene is low to undetectable in resting T and B lymphocytes and shows a biphasic induction in both cell types after mitogenic stimulation, with a first peak at 3 hours and a second and stronger induction at 44 to 72 hours. Study of the B-myb gene showed that this gene is low to undetectable in resting T or B cells and is strongly induced after mitogenic stimulation with a peak between 44 and 72 hours in both cell types. Finally, the A-myb gene shows a pattern of expression in lymphocytes different from that of c- myb and B-myb. It is expressed in resting T lymphocytes and its levels gradually decrease after mitogenic stimulation to become undetectable at 48 hours. It is also expressed in a subpopulation of large B lymphocytes but not in in vitro activated B cells. Neither of the three members of the myb family of genes was expressed in monocytes and granulocytes, even after functional activation of these cells. Taken together, these data bring further evidence for the role of c-myb in cellular proliferation and on the basis of the kinetics of its induction relative to thymidine uptake, we hypothesize that it may have a role during G1 progression in addition to that already documented for entry into S phase. Furthermore, our studies indicate that another member of the myb family of genes, B-myb, may also be involved in cellular proliferation, because its expression correlates with the induction of mitogenesis.


2014 ◽  
Vol 95 (6) ◽  
pp. 1307-1319 ◽  
Author(s):  
Ernest T. Chivero ◽  
Nirjal Bhattarai ◽  
Robert T. Rydze ◽  
Mark A. Winters ◽  
Mark Holodniy ◽  
...  

Human pegivirus (HPgV; previously called GB virus C/hepatitis G virus) has limited pathogenicity, despite causing persistent infection, and is associated with prolonged survival in human immunodeficiency virus-infected individuals. Although HPgV RNA is found in and produced by T- and B-lymphocytes, the primary permissive cell type(s) are unknown. We quantified HPgV RNA in highly purified CD4+ and CD8+ T-cells, including naïve, central memory and effector memory populations, and in B-cells (CD19+), NK cells (CD56+) and monocytes (CD14+) using real-time reverse transcription-PCR. Single-genome sequencing was performed on viruses within individual cell types to estimate genetic diversity among cell populations. HPgV RNA was present in CD4+ and CD8+ T-lymphocytes (nine of nine subjects), B-lymphocytes (seven of ten subjects), NK cells and monocytes (both four of five). HPgV RNA levels were higher in naïve (CD45RA+) CD4+ cells than in central memory and effector memory cells (P<0.01). HPgV sequences were highly conserved among subjects (0.117±0.02 substitutions per site; range 0.58–0.14) and within subjects (0.006±0.003 substitutions per site; range 0.006–0.010). The non-synonymous/synonymous substitution ratio was 0.07, suggesting a low selective pressure. Carboxyfluorescein succinimidyl ester (CFSE)-labelled HPgV RNA-containing particles precipitated by a commercial exosome isolation reagent delivered CSFE to uninfected monocytes, NK cells and T- and B-lymphocytes, and HPgV RNA was transferred to PBMCs with evidence of subsequent virus replication. Thus, HPgV RNA-containing serum particles including microvesicles may contribute to delivery of HPgV to PBMCs in vivo, explaining the apparent broad tropism of this persistent human RNA virus.


Blood ◽  
1991 ◽  
Vol 77 (1) ◽  
pp. 149-158 ◽  
Author(s):  
J Golay ◽  
A Capucci ◽  
M Arsura ◽  
M Castellano ◽  
V Rizzo ◽  
...  

The steady-state expression of three members of the myb family of genes, c-myb, B-myb, and A-myb, was studied in four purified normal human hematopoietic cell types, ie, T and B lymphocytes, monocytes, and granulocytes. The c-myb proto-oncogene is low to undetectable in resting T and B lymphocytes and shows a biphasic induction in both cell types after mitogenic stimulation, with a first peak at 3 hours and a second and stronger induction at 44 to 72 hours. Study of the B-myb gene showed that this gene is low to undetectable in resting T or B cells and is strongly induced after mitogenic stimulation with a peak between 44 and 72 hours in both cell types. Finally, the A-myb gene shows a pattern of expression in lymphocytes different from that of c- myb and B-myb. It is expressed in resting T lymphocytes and its levels gradually decrease after mitogenic stimulation to become undetectable at 48 hours. It is also expressed in a subpopulation of large B lymphocytes but not in in vitro activated B cells. Neither of the three members of the myb family of genes was expressed in monocytes and granulocytes, even after functional activation of these cells. Taken together, these data bring further evidence for the role of c-myb in cellular proliferation and on the basis of the kinetics of its induction relative to thymidine uptake, we hypothesize that it may have a role during G1 progression in addition to that already documented for entry into S phase. Furthermore, our studies indicate that another member of the myb family of genes, B-myb, may also be involved in cellular proliferation, because its expression correlates with the induction of mitogenesis.


2017 ◽  
Vol 2 (3) ◽  
Author(s):  
Flavia Novelli ◽  
Monia Vadrucci ◽  
Maria Manuela Rosado ◽  
Luigi Picardi ◽  
Eugenio Benvenuto ◽  
...  

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