| First Author | Martinez HG | Year | 2012 |
| Journal | BMC Immunol | Volume | 13 |
| Pages | 56 | PubMed ID | 23074996 |
| Mgi Jnum | J:318161 | Mgi Id | MGI:6858514 |
| Doi | 10.1186/1471-2172-13-56 | Citation | Martinez HG, et al. (2012) Important role of CCR2 in a murine model of coronary vasculitis. BMC Immunol 13:56 |
| abstractText | BACKGROUND: Chemokines and their receptors play a role in the innate immune response as well as in the disruption of the balance between pro-inflammatory Th17 cells and regulatory T cells (Treg), underlying the pathogenesis of coronary vasculitis in Kawasaki disease (KD). RESULTS: Here we show that genetic inactivation of chemokine receptor (CCR)-2 is protective against the induction of aortic and coronary vasculitis following injection of Candida albicans water-soluble cell wall extracts (CAWS). Mechanistically, both T and B cells were required for the induction of vasculitis, a role that was directly modulated by CCR2. CAWS administration promoted mobilization of CCR2-dependent inflammatory monocytes (iMo) from the bone marrow (BM) to the periphery as well as production of IL-6. IL-6 was likely to contribute to the depletion of Treg and expansion of Th17 cells in CAWS-injected Ccr2(+/+) mice, processes that were ameliorated following the genetic inactivation of CCR2. CONCLUSION: Collectively, our findings provide novel insights into the role of CCR2 in the pathogenesis of vasculitis as seen in KD and highlight novel therapeutic targets, specifically for individuals resistant to first-line treatments. |
