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  Enhanced B-cell activation mediated by TLR4 and BCR crosstalk

Minguet, S., Dopfer, E. P., Pollmer, C., Freudenberg, M. A., Galanos, C., Reth, M., et al. (2008). Enhanced B-cell activation mediated by TLR4 and BCR crosstalk. European Journal of Immunology, 38, 2475-2487.

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 Creators:
Minguet, Susana1, Author
Dopfer, Elaine P.2, Author              
Pollmer, Careen2, Author              
Freudenberg, Marina A.3, Author              
Galanos, Chris4, Author              
Reth, Michael2, Author              
Huber, Michael2, Author              
Schamel, Wolfgang W.2, Author              
Affiliations:
1Max Planck Society, ou_persistent13              
2Research Group and Chair of Molecular Immunology of the University of Freiburg, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243645              
3Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
4Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              

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Free keywords: BCR; B lymphocytes; CD69; Lipopolysaccharide; TLR4
 Abstract: Despite the important role of B lymphocytes as a bridge between the innate and the adaptive immune system, little is known regarding lipopolysaccharide (LPS) recognition, activation of signalling networks or conceivable cooperation between LPS and the B-cell antigen receptor (BCR). Here, we show that primary B cells can efficiently discriminate between different LPS chemotypes, responding with at least 100-fold higher sensitivity to rough-form LPS compared with smooth-form LPS. Using genetically modified mice, we demonstrate that B lymphocytes recognize all LPS chemotypes via Toll-like receptor 4 (TLR4). In addition, we dissect the signalling pathways that lead to CD69 upregulation upon TLR4 and BCR activation in primary B cells. Our data suggest that TLR4 and BCR induce CD69 transcription via two distinct sets of signalling molecules, exerting quantitative and qualitative differences in B-cell activation. Finally, we show that simultaneous stimulation of TLR4 and BCR additively elevates B-cell activation. In contrast, co-engagement of TLR4 and BCR by antigen-coupled LPS synergistically enhances activation of B cells, pointing out attractive targets for signalling crosstalk in B lymphocytes.

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Language(s): eng - English
 Dates: 2008
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: eDoc: 401207
 Degree: -

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Title: European Journal of Immunology
  Alternative Title : Eur. J. Immunol.
Source Genre: Journal
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Pages: - Volume / Issue: 38 Sequence Number: - Start / End Page: 2475 - 2487 Identifier: -