| First Author | Carrithers MD | Year | 2002 |
| Journal | J Neuroimmunol | Volume | 129 |
| Issue | 1-2 | Pages | 51-7 |
| PubMed ID | 12161020 | Mgi Jnum | J:102957 |
| Mgi Id | MGI:3608270 | Doi | 10.1016/s0165-5728(02)00172-8 |
| Citation | Carrithers MD, et al. (2002) Role of genetic background in P selectin-dependent immune surveillance of the central nervous system. J Neuroimmunol 129(1-2):51-7 |
| abstractText | Although the blood-brain barrier and blood cerebrospinal fluid barrier maintain the central nervous system (CNS) as an immunologically privileged site, T lymphocytes can migrate through unstimulated brain endothelium and epithelium to perform immune surveillance or initiate inflammation. Our prior results suggested that early CNS migration of a CD4 Th1 cell line was facilitated by P selectin (CD62P) in (PL/JxSJL/J)F1 mice. Here, quantitative analysis of migration 2 h following adoptive transfer of fluorescently labeled cells revealed a 53-72% decrease in activated splenocyte, CD4 Th1 and CD8 migration, but not CD4 Th2, in CD62P-deficient C57BL6/J mice. Immunohistochemistry revealed constitutive expression of CD62P within the meninges and choroid plexus epithelia in C57BL6/J and SJL/J, but not BALB/cJ, mice. Activated splenocyte migration was approximately three- to four-fold greater in SJL/J as compared to BALB/cJ mice. Anti-CD62P treatment normalized this difference. Based on these results, we hypothesize that genetically determined kinetics of immune surveillance may regulate the phenotype of subsequent CNS inflammation. |
