EXPRESSION OF ICAM-1, VCAM-1, L-SELECTIN, AND LEUKOSIALIN IN THE MOUSE CENTRAL-NERVOUS-SYSTEM DURING THE INDUCTION AND REMISSION STAGES OF EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS

Adhesion molecules facilitate infiltration of leukocytes into the cent ral nervous system (CNS) of mice with experimental allergic encephalom yelitis (EAE). Expression of the adhesion molecules ICAM-1 (CD54), VCA M-1 (CD106), L-selectin (CD62L), and leukosialin (CD43) was analyzed v ia immunocytochemistry 4-28 days after the injection of encephalitogen into EAE-susceptible SWXJ mice. Constitutive ICAM-1 expression on lar ge-diameter CNS vessels was upregulated on post-injection days 8, 11, 14 and 18 (concurrent with de novo expression on smaller capillaries a nd glial cells), partially downregulated by day 23, and back to contro l levels by day 28. Constitutive VCAM-1 expression was upregulated by day 14 and back to control levels by day 28. Upregulation of ICAM-1 te mporally coincided with the immigration of CD4(+) lymphocytes and L-se lectin(+) leukocytes into the CNS, while downregulation coincided with their emigration. The infiltration of CD43(+) leukocytes also coincid ed with the upregulation of vascular adhesion molecules, but CD43(+) c ells remained in the CNS after ICAM-1 and VCAM-1 had returned to contr ol levels. Cellular infiltration and adhesion-molecule expression prec eded EAE clinical symptoms by a minimum of 3 days, suggesting a causal role of adhesion molecules in the initiation of CNS inflammation. How ever, prophylactic injections of monoclonal antibodies against either ICAM-1, L-selectin, or CD43, did not ameliorate the clinical severity of EAE in this model.