scholarly journals Characterization of Human B-Cell Lines Harbouring Both Adult T-Cell Leukaemia (ATL) Virus and Epstein--Barr Virus Derived from ATL Patients

1984 ◽  
Vol 65 (10) ◽  
pp. 1781-1789 ◽  
Author(s):  
Y. Koyanagi ◽  
N. Yamamoto ◽  
N. Kobayashi ◽  
K. Hirai ◽  
H. Konishi ◽  
...  
1985 ◽  
Vol 5 (5) ◽  
pp. 340-344 ◽  
Author(s):  
Dimitrios T. Boumpas ◽  
John J. Hooks ◽  
Mikulas Popovic ◽  
George C. Tsokos ◽  
Dean L. Mann

2001 ◽  
Vol 75 (8) ◽  
pp. 3740-3752 ◽  
Author(s):  
Sarah Nikiforow ◽  
Kim Bottomly ◽  
George Miller

ABSTRACT In immunodeficient hosts, Epstein-Barr virus (EBV) often induces extensive B-cell lymphoproliferative disease and lymphoma. Without effective in vitro immune surveillance, B cells infected by the virus readily form immortalized cell lines. In the regression assay, memory T cells inhibit the formation of foci of EBV-transformed B cells that follows recent in vitro infection by EBV. No one has yet addressed which T cell regulates the early proliferative phase of B cells newly infected by EBV. Using new quantitative methods, we analyzed T-cell surveillance of EBV-mediated B-cell proliferation. We found that CD4+ T cells play a significant role in limiting proliferation of newly infected, activated CD23+ B cells. In the absence of T cells, EBV-infected CD23+ B cells divided rapidly during the first 3 weeks after infection. Removal of CD4+ but not CD8+ T cells also abrogated immune control. Purified CD4+ T cells eliminated outgrowth when added to EBV-infected B cells. Thus, unlike the killing of EBV-infected lymphoblastoid cell lines, in which CD8+ cytolytic T cells play an essential role, prevention of early-phase EBV-induced B-cell proliferation requires CD4+ effector T cells.


1982 ◽  
Vol 156 (3) ◽  
pp. 930-935 ◽  
Author(s):  
N Chiorazzi ◽  
R L Wasserman ◽  
H G Kunkel

HGPRTase-deficient EBV-transformed B cell lines were shown to be effective fusion partners with mitogen-activated human B cells for the construction of Ig-producing human B cell hybridomas. In a series of experiments using these lines and B cells from several tissue sources, approximatley 20% of the cultures plated were consistently positive for growth after hypoxanthine-aminopterin-thymidine selection and approximatley 30% of these synthesized significant new Ig. A marked increase in Ig secretion was observed after hybridization, which was due to new Ig; Ig from the parental lime was shown to disappear in several instances. Special analyses were carried out on a human hybridoma secreting antibody specific for tetanus toxoid and tetanus toxin and stable subclones were derived. These studies suggest that EBV-transformed lines will prove useful in human hybridization studies, thus making a large library of B cell lines available for the generation of human monoclonal antibodies.


1997 ◽  
Vol 10 (4) ◽  
pp. 183-195 ◽  
Author(s):  
ROSEMARY ROCHFORD ◽  
MARTIN J. CANNON ◽  
REBECCA E. SABBE ◽  
KALYANI ADUSUMILLI ◽  
GASTON PICCHIO ◽  
...  

1993 ◽  
Vol 177 (2) ◽  
pp. 295-304 ◽  
Author(s):  
N Burdin ◽  
C Péronne ◽  
J Banchereau ◽  
F Rousset

Interleukin 10 (IL-10) is a pleiotropic factor that enhances proliferation of activated human B lymphocytes and induces them to secrete high amounts of immunoglobulins. Here we show that several human B cell lines were able to constitutively secrete human (h)IL-10. Whereas none of the pre-B nor the plasmocytic cell lines tested produced hIL-10, 25 of the 36 tested mature B cell lines (lymphoblastoid and Burkitt lymphoma cell lines) secreted hIL-10. Moreover, 24 of these 25 hIL-10-producing B cell lines contained the Epstein-Barr virus (EBV) genome, suggesting a relationship between hIL-10 production by human B cell lines and EBV expression. Accordingly, whereas polyclonal activation via triggering of surface immunoglobulins or CD40 antigen induced highly purified normal human B lymphocytes to produce only low (0.3-0.4 ng/ml) but significant amounts of hIL-10, EBV infection induced them to secrete high amounts of hIL-10 (4-9 ng/ml). Furthermore, addition of exogenous hIL-10, simultaneously to EBV infection, potentiated cell proliferation, whereas a blocking anti-IL-10 antiserum inhibited it. Thus, hIL-10 produced by infected human B lymphocytes appears to be involved in the mechanisms of EBV-induced B cell proliferation.


1990 ◽  
Vol 60 (3) ◽  
pp. 206-212
Author(s):  
Ottmar Janssen ◽  
Barbara Heinze ◽  
Claus R. Bartram ◽  
Michael Pawlita ◽  
Thomas Binder ◽  
...  

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