| First Author | Fife BT | Year | 2000 |
| Journal | J Exp Med | Volume | 192 |
| Issue | 6 | Pages | 899-905 |
| PubMed ID | 10993920 | Mgi Jnum | J:64904 |
| Mgi Id | MGI:1890105 | Doi | 10.1084/jem.192.6.899 |
| Citation | Fife BT, et al. (2000) CC chemokine receptor 2 is critical for induction of experimental autoimmune encephalomyelitis. J Exp Med 192(6):899-906 |
| abstractText | Experimental autoimmune encephalomyelitis (EAE) is a CD4(+) T lymphocyte-mediated disease of the central nervous system (CNS) characterized by mononuclear cell infiltration, demyelination, and paralysis. We previously demonstrated a role for chemokines in acute and relapsing EAE pathogenesis. Presently, we investigated the role of CC chemokine receptor 2 (CCR2) in acute EAE. CCR2(-/)- mice did not develop clinical EAE or CNS histopathology, and showed a significant reduction in T cell- and CNS-infiltrating CD45(high)F4/80(+) monocyte subpopulations. Peripheral lymphocytes from CCR2(-/)- mice produced comparable levels of interferon-gamma (IFN-gamma) and interleukin (IL)-2 in response to antigen-specific restimulation when compared with control mice. Adoptively transferred myelin oligodendrocyte glycoprotein 35-55-specific T cells lacking expression of CCR2 were able to induce EAE, whereas CCR2(-/)- recipients of wild-type T cells failed to develop disease. These results suggest that CCR2 expression on host-derived mononuclear cells is critical for disease induction. |
