| First Author | Gonnella PA | Year | 2003 |
| Journal | J Immunol | Volume | 170 |
| Issue | 5 | Pages | 2316-22 |
| PubMed ID | 12594253 | Mgi Jnum | J:82016 |
| Mgi Id | MGI:2450514 | Doi | 10.4049/jimmunol.170.5.2316 |
| Citation | Gonnella PA, et al. (2003) Induction of low dose oral tolerance in monocyte chemoattractant protein-1- and CCR2-deficient mice. J Immunol 170(5):2316-22 |
| abstractText | The chemokine monocyte chemoattractant protein-1 (MCP-1) and its receptor CCR2 have been shown to play an important role in the migration and trafficking of macrophages and Th1 effector cells in experimental autoimmune encephalomyelitis. Also, MCP-1 has been reported to regulate oral tolerance induction by inhibition of Th1 cell-related cytokines and by the ability of Abs to MCP-1 to inhibit oral tolerance. This study demonstrates that neither MCP-1 nor its receptor CCR2 is required for the induction of oral tolerance. Mice deletional for either MCP-1 or CCR2 had suppressed cell-proliferative and Th1 responses following oral administration and immunization with myelin oligodendrocyte glycoprotein (MOG(35-55)). TGF-beta was up-regulated in fed and immunized deletional mice, while IL-4 was absent from deletional mice, but up-regulated in controls. Decreased experimental autoimmune encephalomyelitis severity was found in MOG(35-55)-fed MCP-1 deletional mice, indicating induction of oral tolerance. These results demonstrate that MCP-1 is not required for induction of oral tolerance and that MCP-1 and CCR2 are essential for up-regulation of IL-4 in tolerized mice. |
