| First Author | Barin JG | Year | 2012 |
| Journal | Eur J Immunol | Volume | 42 |
| Issue | 3 | Pages | 726-36 |
| PubMed ID | 22161142 | Mgi Jnum | J:187791 |
| Mgi Id | MGI:5438193 | Doi | 10.1002/eji.201141737 |
| Citation | Barin JG, et al. (2012) Macrophages participate in IL-17-mediated inflammation. Eur J Immunol 42(3):726-36 |
| abstractText | The involvement of macrophages (MPhis) in Th17-cell responses is still poorly understood. While neutrophils are thought to be the predominant effector of Th17-cell responses, IL-17 is also known to induce myelotropic chemokines and growth factors. Other T-cell-derived cytokines induce non-classical functions, suggesting that IL-17 sigxnaling may similarly elicit unique MPhi functions. Here, we characterized the expression of subunits of the IL-17 receptor on primary murine MPhis from different anatomical compartments. The greatest expression of IL-17 receptors was observed on mucosal Ly6C(hi) "inflammatory" MPhis. We further observed upregulation of IL-17 receptors in vitro on bone marrow-derived macrophages (BMMPhis) in response to peptidoglycan or CpG oligonucleotide stimuli, and in vivo, upon CFA administration. Macrophages expressing IL-17 receptors were observed infiltrating the hearts of mice with myocarditis, and genetic ablation of IL-17RA altered MPhi recruitment. Treating primary MPhis from a wide variety of different anatomic sources (as well as cell lines) with IL-17A induced the production of unique profiles of cytokines and chemokines, including GM-CSF, IL-3, IL-9, CCL4/MIP-1beta and CCL5/RANTES. IL-17A also induced production of IL-12p70; IL-17-signaling-deficient MPhis elicited diminished IFN-gamma production by responding DO11.10 CD4(+) T cells when used as APCs. These data indicate that MPhis from different anatomic locations direct IL-17-mediated responses. |
