Journal of Neuroimmunology, Vol. 129 (1-2) (2002) pp. 51-57
Michael D. Carrithers * a,b, Irene Visintin a, Christophe Viret a and Charles A. Janeway Jr. a,c
a Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520-0811, USA
b Department of Neurology, Yale University School of Medicine, New Haven, CT 06520, USA
c Howard Hughes Medical Institute, Yale University School of Medicine, New Haven, CT 06520, USA
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/J×SJL/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.
© 2002 Elsevier Science B.V.