| First Author | Mancardi DA | Year | 2011 |
| Journal | J Immunol | Volume | 186 |
| Issue | 4 | Pages | 1899-903 |
| PubMed ID | 21248252 | Mgi Jnum | J:169145 |
| Mgi Id | MGI:4939946 | Doi | 10.4049/jimmunol.1003642 |
| Citation | Mancardi DA, et al. (2011) The murine high-affinity IgG receptor Fc(gamma)RIV is sufficient for autoantibody-induced arthritis. J Immunol 186(4):1899-903 |
| abstractText | K/BxN serum-induced passive arthritis was reported to depend on the activation of mast cells, triggered by the activating IgG receptor FcgammaRIIIA, when engaged by IgG1 autoantibodies present in K/BxN serum. This view is challenged by the fact that FcgammaRIIIA-deficient mice still develop K/BxN arthritis and because FcgammaRIIIA is the only activating IgG receptor expressed by mast cells. We investigated the contribution of IgG receptors, IgG subclasses, and cells in K/BxN arthritis. We found that the activating IgG2 receptor FcgammaRIV, expressed only by monocytes/macrophages and neutrophils, was sufficient to induce disease. K/BxN arthritis occurred not only in mast cell-deficient W(sh) mice, but also in mice whose mast cells express no activating IgG receptors. We propose that at least two autoantibody isotypes, IgG1 and IgG2, and two activating IgG receptors, FcgammaRIIIA and FcgammaRIV, contribute to K/BxN arthritis, which requires at least two cell types other than mast cells, monocytes/macrophages, and neutrophils. |
