The human Burkitt lymphoma cell line Namalwa represents a homogenous cell system characterized by high levels of Toll-like receptor 9 and activation by CpG oligonucleotides
Human B cells and plasmacytoid dendritic cells constitutively express Toll-like receptor (TLR)9 and respond to TLR9 ligands, as evidenced by nuclear factor kappa B translocation and cytokine secretion. However, TLR9 expression on B lymphocytes appears to be dependent upon both the state of activatio...
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Published in | Journal of immunological methods Vol. 300; no. 1; pp. 93 - 99 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Amsterdam
Elsevier B.V
01.05.2005
Elsevier |
Subjects | |
Online Access | Get full text |
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Summary: | Human B cells and plasmacytoid dendritic cells constitutively express Toll-like receptor (TLR)9 and respond to TLR9 ligands, as evidenced by nuclear factor kappa B translocation and cytokine secretion. However, TLR9 expression on B lymphocytes appears to be dependent upon both the state of activation and differentiation of the B cell population. In the current study, TLR9 mRNA expression was evaluated in transformed human B cell lines and correlated with their response to CpG. Among the B cell lines, the Burkitt lymphoma-derived Namalwa line had the highest level of TLR9 expression, 20-fold greater than spleen. Following incubation with CpG oligonucleotide, Namalwa cells secreted increased amounts of TNF, IL-6, and IL-10 and expressed the costimulator molecules CD40, CD80, and CD86. These functional responses to TLR9 activation occurred with similar EC
50 values in the 30- to 60-nM range. These results suggest that the Namalwa Burkitt lymphoma line may serve as a useful cell-based assay for the detection of novel TLR9 agonists as well as a model to further explore the regulation of TLR9 expression and signaling. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0022-1759 1872-7905 |
DOI: | 10.1016/j.jim.2005.02.012 |