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CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses

Diego Mourão-Sá, Matthew J Robinson, Santiago Zelenay, David Sancho, Probir Chakravarty, Rasmus Larsen, Maud Plantinga, Nico Van Rooijen, Miguel P Soares, Bart Lambrecht UGent, et al. (2011) EUROPEAN JOURNAL OF IMMUNOLOGY. 41(10). p.3040-3053
abstract
Myeloid cells express a plethora of C-type lectin receptors (CLRs) that can regulate immune responses. CLEC-2 belongs to the Dectin-1 sub-family of CLRs that possess an extracellular C-type lectin-like domain and a single intracellular hemITAM motif. CLEC-2 is highly expressed on mouse and human platelets where it signals via Syk to promote aggregation. We generated a monoclonal antibody (mAb) against mouse CLEC-2 and found that CLEC-2 is additionally widely expressed on leukocytes and that its expression is upregulated during inflammation. MAb-mediated crosslinking of CLEC-2 leads to hemITAM- dependent signaling via Syk, Ca(2+) and NFAT and, in myeloid cells, modulates the effect of toll-like receptor (TLR) agonists to selectively potentiate production of IL-10. A macrophage/dendritic cell-dependent increase in IL-10 is also observed in mice given anti-CLEC-2 mAb together with LPS. Collectively, these data indicate that CLEC-2 is expressed in myeloid cells and acts as a Syk-coupled CLR able to modulate TLR signaling and inflammatory responses.
Please use this url to cite or link to this publication:
author
organization
year
type
journalArticle (original)
publication status
published
subject
keyword
HemITAM, IL-10, C-type lectin, CLEC-2, Syk, C-TYPE LECTIN, BETA-GLUCAN RECOGNITION, DENDRITIC CELLS, PLATELET ACTIVATION, RECEPTOR CLEC-2, CELLULAR ACTIVATION, CYTOKINE PRODUCTION, FUNGAL-INFECTIONS, CANDIDA-ALBICANS, INNATE IMMUNITY
journal title
EUROPEAN JOURNAL OF IMMUNOLOGY
Eur. J. Immunol.
volume
41
issue
10
pages
3040 - 3053
Web of Science type
Article
Web of Science id
000296199000026
JCR category
IMMUNOLOGY
JCR impact factor
5.103 (2011)
JCR rank
24/138 (2011)
JCR quartile
1 (2011)
ISSN
0014-2980
DOI
10.1002/eji.201141641
language
English
UGent publication?
yes
classification
A1
copyright statement
I have transferred the copyright for this publication to the publisher
id
2002891
handle
http://hdl.handle.net/1854/LU-2002891
date created
2012-01-25 12:21:49
date last changed
2016-12-19 15:42:53
@article{2002891,
  abstract     = {Myeloid cells express a plethora of C-type lectin receptors (CLRs) that can regulate immune responses. CLEC-2 belongs to the Dectin-1 sub-family of CLRs that possess an extracellular C-type lectin-like domain and a single intracellular hemITAM motif. CLEC-2 is highly expressed on mouse and human platelets where it signals via Syk to promote aggregation. We generated a monoclonal antibody (mAb) against mouse CLEC-2 and found that CLEC-2 is additionally widely expressed on leukocytes and that its expression is upregulated during inflammation. MAb-mediated crosslinking of CLEC-2 leads to hemITAM- dependent signaling via Syk, Ca(2+) and NFAT and, in myeloid cells, modulates the effect of toll-like receptor (TLR) agonists to selectively potentiate production of IL-10. A macrophage/dendritic cell-dependent increase in IL-10 is also observed in mice given anti-CLEC-2 mAb together with LPS. Collectively, these data indicate that CLEC-2 is expressed in myeloid cells and acts as a Syk-coupled CLR able to modulate TLR signaling and inflammatory responses.},
  author       = {Mour{\~a}o-S{\'a}, Diego and Robinson, Matthew J and Zelenay, Santiago and Sancho, David and Chakravarty, Probir and Larsen, Rasmus and Plantinga, Maud and Van Rooijen, Nico and Soares, Miguel P and Lambrecht, Bart and Reis e Sousa, Caetano},
  issn         = {0014-2980},
  journal      = {EUROPEAN JOURNAL OF IMMUNOLOGY},
  keyword      = {HemITAM,IL-10,C-type lectin,CLEC-2,Syk,C-TYPE LECTIN,BETA-GLUCAN RECOGNITION,DENDRITIC CELLS,PLATELET ACTIVATION,RECEPTOR CLEC-2,CELLULAR ACTIVATION,CYTOKINE PRODUCTION,FUNGAL-INFECTIONS,CANDIDA-ALBICANS,INNATE IMMUNITY},
  language     = {eng},
  number       = {10},
  pages        = {3040--3053},
  title        = {CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses},
  url          = {http://dx.doi.org/10.1002/eji.201141641},
  volume       = {41},
  year         = {2011},
}

Chicago
Mourão-Sá, Diego, Matthew J Robinson, Santiago Zelenay, David Sancho, Probir Chakravarty, Rasmus Larsen, Maud Plantinga, et al. 2011. “CLEC-2 Signaling via Syk in Myeloid Cells Can Regulate Inflammatory Responses.” European Journal of Immunology 41 (10): 3040–3053.
APA
Mourão-Sá, D., Robinson, M. J., Zelenay, S., Sancho, D., Chakravarty, P., Larsen, R., Plantinga, M., et al. (2011). CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses. EUROPEAN JOURNAL OF IMMUNOLOGY, 41(10), 3040–3053.
Vancouver
1.
Mourão-Sá D, Robinson MJ, Zelenay S, Sancho D, Chakravarty P, Larsen R, et al. CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses. EUROPEAN JOURNAL OF IMMUNOLOGY. 2011;41(10):3040–53.
MLA
Mourão-Sá, Diego, Matthew J Robinson, Santiago Zelenay, et al. “CLEC-2 Signaling via Syk in Myeloid Cells Can Regulate Inflammatory Responses.” EUROPEAN JOURNAL OF IMMUNOLOGY 41.10 (2011): 3040–3053. Print.