TLR Stimulation Modifies BLyS Receptor Expression in Follicular and Marginal Zone B Cells

Through their differential interactions with B lymphocyte stimulator (BLyS) and a proliferation-inducing ligand (APRIL), the three BLyS family receptors play central roles in B cell survival and differentiation. Recent evidence indicates BLyS receptor levels shift following BCR ligation, suggesting...

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Bibliographic Details
Published in:Journal of Immunology 2007-06, Vol.178 (12), p.7531-7539
Main Authors: Treml, Laura S, Carlesso, Gianluca, Hoek, Kristen L, Stadanlick, Jason E, Kambayashi, Taku, Bram, Richard J, Cancro, Michael P, Khan, Wasif N
Format: Article
Language:English
Subjects:
Animals
B-Cell Activation Factor Receptor - metabolism
B-Lymphocytes - immunology
Lipopolysaccharides - pharmacology
Mice
Mice, Inbred C57BL
Myeloid Differentiation Factor 88 - metabolism
Oligodeoxyribonucleotides - pharmacology
Proto-Oncogene Proteins c-rel - metabolism
Receptors, Tumor Necrosis Factor - metabolism
Toll-Like Receptor 4 - agonists
Toll-Like Receptor 9 - agonists
Transmembrane Activator and CAML Interactor Protein - metabolism
Tumor Necrosis Factor Ligand Superfamily Member 13 - metabolism
Up-Regulation
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Summary:Through their differential interactions with B lymphocyte stimulator (BLyS) and a proliferation-inducing ligand (APRIL), the three BLyS family receptors play central roles in B cell survival and differentiation. Recent evidence indicates BLyS receptor levels shift following BCR ligation, suggesting that activation cues can alter overall BLyS receptor profiles and thus ligand sensitivity. In this study, we show that TLR stimuli also alter BLyS receptor expression, but in contrast to BCR ligation, TLR9 and TLR4 signals, preferentially increase transmembrane activator calcium modulator and cyclophilin ligand interactor (TACI) expression. Although both of these TLRs act through MyD88-dependent mechanisms to increase TACI expression, they differ in terms of their downstream mediators and the B cell subset affected. Surprisingly, only TLR4 relies on c-Rel and p50 to augment TACI expression, whereas TLR9 does not. Furthermore, although all follicular and marginal zone B cells up-regulate TACI in response to TLR9 stimulation, only marginal zone B cells and a subset of follicular B cells respond to TLR4. Finally, we find that both BLyS and APRIL enhance viability among quiescent and BCR-stimulated B cells. However, although BLyS enhances viability among TLR stimulated B cells, APRIL does not, suggesting that TACI but not BLyS receptor 3 may share survival promoting pathways with TLRs.
ISSN:0022-1767
1550-6606
1365-2567
DOI:10.4049/jimmunol.178.12.7531