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
Jm. Dopp et al., 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, Journal of neuroimmunology, 54(1-2), 1994, pp. 129-144
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.