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BJAb (EBV- negative, Burkitt- like lymphoma)

BJAb (EBV- negative, Burkitt- like lymphoma) - Cell Biology and Cell Culture

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Old 07-09-2008, 01:03 PM
Kym Hall
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Default BJAb (EBV- negative, Burkitt- like lymphoma)



Did you get any answers to your question about the origin of the Bjab cell
line?


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Old 09-12-2012, 08:15 AM
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Default Re: BJAb (EBV- negative, Burkitt- like lymphoma)

BJAB (EBV-negative) is African Burkitt lymphoma cell lines from peripheral blood B lymphocytes. Working in 2004 at Institut National de Recherche Biomédicales (Kinshasa - RDC) directed by Jean-Jacques Muyembe-Tamfum PhD, I have opportunity to examine Raji cellular lines of Burkitt lymphoma from peripheral blood B lymphocytes, positive EA-EBV, by teenager, that have been maintained, such as BJAB cell line, in RPMI 1640 medium supplemented with 2 mM L-glutamine, penicillin (50 units/ml), streptomycin sulfate (50 ug/ml), and 10% (vol/vol) heat-inactivated newborn calf serum at 37 °C in an atmosphere of 5% CO2. Phorbol 12-myristate 13-acetate (" 12-O-tetradecanoyl-phorbol 13-acetate," TPA) at 20 ng/ml was used to activate Raji cells (5 x 10^5 cells per ml) for 3 days at 37 °C.
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Old 09-13-2012, 12:39 PM
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Default Re: BJAb (EBV- negative, Burkitt- like lymphoma)

The natural history of BL (Burkitt's lymphoma) Raji cell line would seem to start after few month from babies birth that they will become one children with latent EBV infection state and malaria resistant. This process through two stages develop one between the ages of 1 to 5, in which they build an immune state to be protected, no against malaria infection but against clinical malaria, so this is a pre-immune stage. The second stage comprehend ages from 5 to 10 in which most surviving children have already acquired a state of clinical immunity protection so it is an immune stage, although protective immunity to malaria infection would never be acquired. EBV lives in the B lymphocytes of 100 % of holoendemic malaria residents in Africa which EBV primary infection is acquired at different ages (during delivery, salivary transmission, etc.) with minor or no clinical signs. Primary EBV infection induces cellular and humoral responses, passing to a latent state during all their lives. Children that survive and reach the second stage will continue being infected by malaria parasites and keep EBV latent infections for all their life. The continue contact with plasmodium expose to develop diseases in which the immune system is involved as result of their continuous antigenic stimulation such as nephrotic syndrome, hyperreactive malaria, splenomegaly, and last but not list BL.
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