| First Author | Lu XJ | Year | 2013 |
| Journal | J Exp Med | Volume | 210 |
| Issue | 1 | Pages | 5-13 |
| PubMed ID | 23254286 | Mgi Jnum | J:194602 |
| Mgi Id | MGI:5474396 | Doi | 10.1084/jem.20121466 |
| Citation | Lu XJ, et al. (2013) LECT2 protects mice against bacterial sepsis by activating macrophages via the CD209a receptor. J Exp Med 210(1):5-13 |
| abstractText | Leukocyte cell-derived chemotaxin 2 (LECT2) is a multifunctional cytokine and reduced plasma levels were found in patients with sepsis. However, precise functions and mechanisms of LECT2 remain unclear. The aim of the present study was to determine the role of LECT2 in modulating immune responses using mouse sepsis models. We found that LECT2 treatment improved outcome in mice with bacterial sepsis. Macrophages (MPhi), but not polymorphonuclear neutrophils, mediated the beneficial effect of LECT2 on bacterial sepsis. LECT2 treatment could alter gene expression and enhance phagocytosis and bacterial killing of MPhi in vitro. CD209a was identified to specifically interact with LECT2 and mediate LECT2-induced MPhi activation. CD209a-expressing MPhi was further confirmed to mediate the effect of LECT2 on sepsis in vivo. Our data demonstrate that LECT2 improves protective immunity in bacterial sepsis, possibly as a result of enhanced MPhi functions via the CD209a receptor. The modulation of MPhi functions by LECT2 may serve as a novel potential treatment for sepsis. |
