Imperial College London

ProfessorVictorTybulewicz

Faculty of MedicineDepartment of Immunology and Inflammation

Visiting Professor
 
 
 
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Contact

 

+44 (0)20 3796 1612v.tybulewicz Website CV

 
 
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Location

 

L2-2720Francis Crick InstituteThe Francis Crick Institute

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Summary

 

Publications

Citation

BibTex format

@article{Schweighoffer:2017:10.1084/jem.20161117,
author = {Schweighoffer, E and Nys, J and Vanes, L and Smithers, N and Tybulewicz, VLJ},
doi = {10.1084/jem.20161117},
journal = {Journal of Experimental Medicine},
title = {TLR4 signals in B lymphocytes are transduced via the B cell antigen receptor and SYK.},
url = {http://dx.doi.org/10.1084/jem.20161117},
volume = {214},
year = {2017}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Toll-like receptors (TLRs) play an important role in immune responses to pathogens by transducing signals in innate immune cells in response to microbial products. TLRs are also expressed on B cells, and TLR signaling in B cells contributes to antibody-mediated immunity and autoimmunity. The SYK tyrosine kinase is essential for signaling from the B cell antigen receptor (BCR), and thus for antibody responses. Surprisingly, we find that it is also required for B cell survival, proliferation, and cytokine secretion in response to signaling through several TLRs. We show that treatment of B cells with lipopolysaccharide, the ligand for TLR4, results in SYK activation and that this is dependent on the BCR. Furthermore, we show that B cells lacking the BCR are also defective in TLR-induced B cell activation. Our results demonstrate that TLR4 signals through two distinct pathways, one via the BCR leading to activation of SYK, ERK, and AKT and the other through MYD88 leading to activation of NF-κB.
AU - Schweighoffer,E
AU - Nys,J
AU - Vanes,L
AU - Smithers,N
AU - Tybulewicz,VLJ
DO - 10.1084/jem.20161117
PY - 2017///
SN - 1540-9538
TI - TLR4 signals in B lymphocytes are transduced via the B cell antigen receptor and SYK.
T2 - Journal of Experimental Medicine
UR - http://dx.doi.org/10.1084/jem.20161117
UR - http://www.ncbi.nlm.nih.gov/pubmed/28356391
UR - http://hdl.handle.net/10044/1/48734
VL - 214
ER -