| CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses. | |
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MedLine Citation:
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PMID: 21728173 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Myeloid cells express a plethora of C-type lectin receptors (CLR) 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 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 toll-like receptor signaling and inflammatory responses. |
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Authors:
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Diego Mourão-Sá; Matthew J Robinson; Santiago Zelenay; David Sancho; Probir Chakravarty; Rasmus Larsen; Maud Plantinga; Nico Van Rooijen; Miguel P Soares; Bart Lambrecht; Caetano Reis E Sousa |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2011-7-4 |
Journal Detail:
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Title: European journal of immunology Volume: - ISSN: 1521-4141 ISO Abbreviation: - Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-7-5 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 1273201 Medline TA: Eur J Immunol Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Copyright Information:
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Copyright © 2011 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim. |
Affiliation:
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Immunobiology Laboratory, Cancer Research UK, London Research Institute, WC2A 3LY London, United Kingdom. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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