| First Author | Mourão-Sá D | Year | 2011 |
| Journal | Eur J Immunol | Volume | 41 |
| Issue | 10 | Pages | 3040-53 |
| PubMed ID | 21728173 | Mgi Jnum | J:176982 |
| Mgi Id | MGI:5293266 | Doi | 10.1002/eji.201141641 |
| Citation | Mourao-Sa D, et al. (2011) CLEC-2 signaling via Syk in myeloid cells can regulate inflammatory responses. Eur J Immunol 41(10):3040-53 |
| abstractText | 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. |
