| First Author | Bullard DC | Year | 2007 |
| Journal | Am J Pathol | Volume | 170 |
| Issue | 6 | Pages | 2001-8 |
| PubMed ID | 17525267 | Mgi Jnum | J:122187 |
| Mgi Id | MGI:3713450 | Doi | 10.2353/ajpath.2007.061016 |
| Citation | Bullard DC, et al. (2007) p150/95 (CD11c/CD18) expression is required for the development of experimental autoimmune encephalomyelitis. Am J Pathol 170(6):2001-8 |
| abstractText | p150/95 (CD11c/CD18, CR4) is a member of the beta(2)-integrin family of adhesion molecules and is considered an important phagocytic receptor. The role of p150/95 in the development of central nervous system demyelinating diseases, including multiple sclerosis, remains unexplored. To determine p150/95-mediated mechanisms in experimental autoimmune encephalomyelitis (EAE), we performed EAE using CD11c-deficient (CD11c(-/-)) mice. EAE in CD11c(-/-) mice was significantly attenuated and characterized by markedly reduced spinal cord T-cell infiltration and interferon-gamma production by these cells. Adoptive transfer of antigen-restimulated T cells from wild-type to CD11c(-/-) mice produced significantly attenuated EAE, whereas transfer of CD11c(-/-) antigen-restimulated T cells to control mice induced a very mild, monophasic EAE. T cells from MOG(35-55) peptide-primed CD11c(-/-) mice displayed an unusual cytokine phenotype with elevated levels of interleukin (IL)-2, IL-4, and IL-12 but reduced levels of interferon-gamma, tumor necrosis factor-alpha, IL-10, IL-17, and transforming growth factor-beta compared with control mice. Overall, CD11c(-/-) T cells from primed mice proliferated comparably to that of control T cells on MOG(35-55) restimulation. Our results indicate that expression of p150/95 is critical on both T cells as well as other leukocytes for the development of demyelinating disease and may represent a novel therapeutic target for multiple sclerosis. |
