| First Author | Reiman R | Year | 2002 |
| Journal | Eur J Immunol | Volume | 32 |
| Issue | 4 | Pages | 1157-63 |
| PubMed ID | 11932923 | Mgi Jnum | J:75976 |
| Mgi Id | MGI:2178171 | Doi | 10.1002/1521-4141(200204)32:4<1157::AID-IMMU1157>3.0.CO;2-M |
| Citation | Reiman R, et al. (2002) Disruption of the C5a receptor gene fails to protect against experimental allergic encephalomyelitis. Eur J Immunol 32(4):1157-63 |
| abstractText | Activation of the complement system generates the anaphylatoxic peptide C5a, which elicits a broad range of inflammatory activities. The biological activities of C5a are mediated through its binding to the widely expressed C5a receptor (C5aR), a G-protein-coupled seven transmembrane domain receptor. In experimental autoimmune encephalomyelitis (EAE), an animal model for multiple sclerosis, the C5aR is expressed on monocytes/macrophages, reactive astrocytes and T cells infiltrating the central nervous system (CNS). To investigate the role of the C5aR in this T cell-driven autoimmunemodel, we induced EAE in C5aR-deficient mice (C5aR(-/-)) and wild-type mice using a myelin oligodendrocyte glycoprotein (MOG) peptide as the immunogen. We found that C5aR(-/-) mice were fully susceptible to MOG-induced EAE with no difference in disease onset or severity in C5aR(-/-) mice compared to control mice. Cellular infiltrates (macrophages and T cells) were similarin the spinal cords of both animal groups and splenic T cells from C5aR(-/-) mice and control mice responded identically to MOG in T cell proliferation assays. Ribonuclease protection assays demonstrated no significant differences in pro-inflammatory gene expression between receptor-deficient and sufficient mice. These results indicate that the C5aR is not an essential mediator in the induction and progression of EAE. |
